Anesthesia Nonanesthetic

NEW DEVELOPMENTS IN MEDICAL RESEARCH
ANESTHESIA FOR
NON-ANESTHESIOLOGISTS
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NEW DEVELOPMENTS IN
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NEW DEVELOPMENTS IN MEDICAL RESEARCH
ANESTHESIA FOR
NON-ANESTHESIOLOGISTS
GREGORY ROSE
AND
J. THOMAS MCLARNEY
EDITORS
Copyright © 2017 by Nova Science Publishers, Inc.
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CONTENTS
Preface vii
Introduction ix
Chapter 1 The Scope of Anesthesia 1
Gregory L. Rose
Chapter 2 Preanesthetic Evaluation 3
J. Thomas McLarney
Chapter 3 Anesthetic Drugs for the Non-Anesthesiologist 23
Jeffrey Oldham
Chapter 4 Pediatric Anesthesia for the Non-Anesthesiologist 37
Raeford E. Brown, Jr.
Chapter 5 Obstetric Anesthesia for the Non-Anesthesiologist 49
Lori C. Kral Barton
Chapter 6 Chronic Pain Management 89
Benjamin J. Sloop
Chapter 7 Anesthesiologist Intensivists: Critical Care
Anesthesiology 95
Habib Srour
Chapter 8 NPO Guidelines 99
Brooke A. Bauer
Chapter 9 The History of Nurse Anesthesia 107
Charles Jonathan Fletcher
vi Contents
Chapter 10 Malignant Hyperthermia, the “Disease of

Anesthesia” 117
Gregory Rose, J. Thomas McLarney, Zaki Hassan
and Raeford Brown
About the Editors 129
List of Contributors 131
Index 133
PREFACE
Anesthesiology is one of the least understood medical specialties. The

drugs and equipment are specialized to a point where physicians in other fields
have little knowledge of how they work. Moreover, the specific techniques
and concerns of anesthesiologists regarding patient care are scarcely known
outside of the specialty.
Most physicians have had a paltry amount of training in anesthesia, if any
at all. Within many medical schools, there is no requirement to rotate in
anesthesiology; if required, the rotation is seen sometimes as a means to
practice intubations and place IVs for a period of two to four weeks, instead of
actually learning anesthesia techniques and practices.
As their role in patient care has stretched outside of the operating room,
anesthesiologists have found that there is often frustration and even conflict in
dealing with other specialties that do not understand the concerns and
necessities that accompany this practice. Why is NPO important? Why does
the patient need to see a cardiologist pre-operatively? Why would the patient
benefit from using Drug A vs Drug B? These questions come up not only in
the operating room, but on the obstetrical floor, in the endoscopy suite, in the
critical care units and elsewhere.
It is the authors’ hope that this book, Anesthesia for Non-
Anesthesiologists, will help to decrease such problems. With chapters written
by a variety of anesthesiologists and subspecialty clinicians at a major
teaching hospital, and edited by experienced academic physicians, the target
audience for this work includes physicians, medical residents, and students
who wish to understand how anesthesiologists think and why they think as
they do.
INTRODUCTION
In our role as academic anesthesiologists, we time and time again

experience the same dilemma; physicians from other specialties, whether
attendings or residents, often do not understand how we approach a patient
who is to be under our care, and why we think the way we do. That is an
understandable situation, seeing as most physicians, when they were in
medical school, had no exposure to an anesthesiology rotation (even though
over the last 10 to 15 years more schools have a required rotation in
anesthesiology). Moreover, many students see an anesthesiology rotation as
simply a chance to intubate and start IVs, and do not try too hard to learn
anesthesia.
The purpose of this book is to therefore explain how we think and why we
think the way we do in a simple format. We are unsure if there are other books
in print that fill this niche, and thus we are excited to have the opportunity to
share this with our colleagues in different specialties.
The editors wish to thank the chapter authors, who squeezed time from a
hectic clinical schedule to write and to re-write their drafts for us. In addition,
we thank our administrative assistant Charles York who has cheerfully been
our proofreader for this work in addition to his other responsibilities.
Greg Rose
Tom McLarney
In: Anesthesia for Non-Anesthesiologists ISBN: 978-1-53611-098-2
Editors: G. Rose and J. T. McLarney © 2017 Nova Science Publishers, Inc.
Chapter 1
THE SCOPE OF ANESTHESIA
Gregory L. Rose, MD
Department of Anesthesiology
University of Kentucky College of Medicine
Lexington, Kentucky, US
What would the practice of modern medicine be like without

anesthesiology? While there are certainly state-of-the-art procedures that do
not require anesthesia, many current medical procedures would be impossible
without anesthesiologists and anesthetists.
Until the mid-1800s, surgical skill was measured not by the outcome, but
by how quickly an awake, restrained, and screaming man’s extremity could be
amputated and cauterized. As another example, appendicitis was very likely a
lethal condition. The surgical knowledge and technique to remove an inflamed
appendix were simple enough, but such an assault on an awake patient might
be fatal. Of course there are reports of surgeries from previous times without
anesthetics, like cutting for the stone (e.g., Samuel Pepys), or Ephraim
McDowell’s successful laparotomy on an awake patient; but such operations
were apparently rare and terrible, or rare and terrible enough that the world
rejoiced when anesthesia was successfully shown to be effective in the 1840s.
The separate, but near-simultaneous clinical use of nitrous oxide and ether
by three men in the 1840s ushered in the United States’ greatest gift to
medicine. Crawford Long, a Georgia physician, had used ether for anesthesia
as early as 1842 but had neglected to publish his experience. Horace Wells
was a dentist from Connecticut who successfully used nitrous oxide for dental
2 Gregory L. Rose
extractions on a series of patients but his demonstration at Massachusetts

General in Boston in 1846 failed when his subject cried out as his tooth was
pulled (even though the subject recalled no pain or awareness during the
procedure). Wells was labeled a failure, and his career and life were ruined.
Later in 1846 William Morton (a dentist and former partner of Wells)
successfully administered ether for a minor surgery at Massachusetts General.
These events sparked a great interest in the concept of anesthesia and clinical
use of ether, nitrous oxide, and later chloroform spread rapidly in both the
United States and Europe. By the time of the American Civil War a decade
and a half later, inhalational anesthesia by ether or chloroform was being used
in field hospitals.
Today, anesthesia is an expected part of most surgical and obstetric
procedures, encompassing general anesthesia, regional anesthesia, local
anesthesia, or sedation. But the practice of anesthesia and anesthesiology is so
much more than the alleviation of consciousness and pain during an operation.
Surgical and obstetric anesthesia is also acute critical care, rendering life
support, volume resuscitation, and mitigating the stress response.
Subspecialties such as cardiothoracic anesthesia, pediatric anesthesia, and
neuroanesthesia focus on the unique challenges of specific physiologic,
pathologic, anatomic, and surgical techniques of each. Likewise, acute and
chronic pain management are individual subspecialties dealing with those
specific problems. Anesthesiologists are active in critical care units,
specifically post-operative care units, because anesthesiologists are best
equipped to manage such patients due to their in-depth knowledge of both
surgical and critical care physiology.
The latest advancement in the scope of anesthesia is the perioperative
surgical home. This concept of patient centered, physician led,
interdisciplinary care illustrates that the anesthesiologist is a true perioperative,
and not simply an intraoperative, physician. Anesthesiologists manage and
coordinate the preoperative care and decision-making processes in preparing a
patient for the operating room, provide intraoperative care, and also provide
postoperative care not only in the recovery room but all through the patient’s
stay. Assisting and/or coordinating the patient’s entire surgical experience
through utilization of evidence-based treatment protocols, the anesthesiologist
works with the surgeon and other consultants, if needed, to medically
maximize the patient for the specific procedure, minimizing surgical delays,
cancellations, and optimizing the quality and timeliness of postoperative care
to avoid known potential complications.
Chapter 2
PREANESTHETIC EVALUATION
J. Thomas McLarney, MD
Anesthesiology Preoperative and Preprocedural Assessment Clinic,
Department of Anesthesiology,
University of Kentucky College of Medicine,
INTRODUCTION
What is the purpose of the preanesthetic evaluation? What’s happening
and what are we doing? Why is it so important? The American Society of
Anesthesiologists (ASA) published a Practice Advisory for Preanesthesia
Evaluation in 2012 to update the original Practice Advisory published in 2002.
In part, the Advisory remarks on content of the preanesthetic evaluation that
includes, but is not limited to, assessment of information from multiple
sources including readily accessible medical records, a patient interview, a
directed preanesthesia examination, preoperative tests when indicated, and
other consultations when appropriate. At a minimum, a directed preanesthetic
physical examination should include an assessment of the airway, lungs, and
heart [1]. While the Advisory provides us with a very nice conceptual
framework for the preanesthetic evaluation and highlights some minimums,
there is much more going on in a preanesthetic evaluation than just satisfying
the minimums, though completion of the minimums is obviously important.
And remember, the evaluation may take place in different places with different
4 J. Thomas McLarney
capabilities and different time constraints. For instance, a preanesthetic

evaluation may be done in a preoperative evaluation clinic for a totally elective
procedure where time and resources are readily available to get outside records
from primary care providers and/or consultants, previous anesthetic records, or
to obtain and review the patient’s medications and allergies, etc. At the other
end of the spectrum the preanesthetic evaluation may be done in the
emergency room as an unconscious patient is being sent emergently to the
operating room, making time and resources to get outside records much more
challenging, if not impossible. The clinical situation, resources at hand and
time sensitivity of the procedure contribute to what can get accomplished in
regard to the preanesthetic evaluation. In this chapter, we will explore the
preanesthetic evaluation, what is being accomplished and why it is so
important.
The preanesthetic evaluation is considered a basic element of anesthetic
care [2]. From the evaluation flows not only answers about the need for
laboratory or other testing, the need for consultations or the need for further
optimization prior to surgery, but also the perioperative/periprocedural
anesthetic plan for the entire episode of care. What type of anesthetic will be
used, general anesthesia versus neuraxial block versus regional anesthesia
versus sedation or a combination? How will the patient be monitored intra-
and postoperatively? How will pain being managed postoperatively? These are
some of the questions being answered from the preanesthetic evaluation. Let
us now briefly discuss the environments in which we complete the
preanesthetic evaluation.
Preanesthetic evaluations take place in several different settings. Most
people probably think first of assessments being done in a dedicated anesthesia
preop clinic for in person evaluations. In person evaluations obviously differ
from phone screens in that a physical examination can be performed.
Generally speaking, in clinic evaluations are usually reserved more for people
with multiple and/or severe comorbidities or for patients having more invasive
procedures. Also, if patients or family members have had problems with
anesthesia in the past, it may be appropriate to see these patients in preop
clinic prior to the day of the procedure if for no other reason than to discuss
what happened, and to validate and address concerns the patient or family has
regarding the anesthetic. It is not uncommon for patients or families to have
significant questions about the risks, benefits and options for their anesthetic
that they would like to discuss with an anesthesiologist prior to the day of the
procedure which may be better served by an in clinic evaluation and
discussion rather than over the phone or even the day of the procedure. In
Preanesthetic Evaluation 5
person evaluations allow for the blink test, or the initial clinical impression
that a provider gets upon walking into the exam room which may or may not
correlate well with the patient on paper. Some people look desperately ill on
paper but when you see them in person they look great and vice versa. These
impressions may have implications for further testing, consultations, or the
anesthetic plan. In clinic evaluations usually afford providers a chance to get
outside records to further complement assessment, optimization and planning.
Interpersonal communication between providers (anesthesiologists, surgeons,
PCP’s, consultants) and patients during this time is invaluable.
Another form of in person evaluation is seeing patients while they are in
the hospital, whether it be the floor, the ICU or the emergency room. The time
sensitive nature of the procedure would once again contribute to how thorough
the evaluation can be. Preanesthetic evaluation the day of the procedure is the
final way we think of doing in person evaluation where resources may be less
well suited to obtain outside records or communicate with PCP’s or
consultants.
Phone screens are another way of assessing patients prior to a procedure
but, as previously stated, do not allow for a physical exam or the blink test.
This method is usually reserved for healthier patients having less invasive
procedures. Usually phone screens are performed by personnel in a preop
clinic so that if it is determined through the course of the phone screen that
they really should be seen in preop clinic that can be readily arranged. As you
can see, triage of who needs to be seen in clinic and who are appropriate for
phone screens is an important part of the preoperative portion of the episode of
care.
We have looked at several parts of the preanesthetic evaluation including
performing a history and physical, gathering outside records, and developing
an anesthetic plan. Other elements that are being completed prior to the day of
the procedure or the day of the procedure include discussions about informed
consent, meaning understanding risks, benefits and options for the anesthetic,
as well as NPO instructions and preop/perioperative medication management
instructions. Establishing trust with the patient and family is also happening
during the time of the preanesthetic evaluation and is an essential part of the
interaction, whether it is before or on the day of the procedure. One final
element of the preanesthetic evaluation that is completed is the ASA Physical
Classification Status, which assigns a number from one to six based on the
health and medical history of the patient (See Table 1). A class 1 patient is a
normal, healthy patient and class 5 patients are not expected to live without an
operation. Class 6 patients have been declared brain dead are going to are
going to have organs removed for the purpose of donation.
Table 1. ASA Physical Status Classification
*
The addition of “E” denotes Emergency surgery: (An emergency is defined as
existing when delay in treatment of the patient would lead to a significant increase
in the threat to life or body part).
ASA Physical Status Classification is reprinted with permission of the American Society of
Anesthesiologists, 1061 American Lane, Schaumburg, Illinois, 60173-4973.
Now that we have reviewed some of the basic concepts and elements of
the preanesthetic evaluation, let us proceed on to some of the individual
elements.
Anesthesiologists love to talk about airway assessment and management
because it is part of what we do every day managing patients. In 2013 the ASA
published updated Practice Guidelines for Management of the Difficult
Airway to update the prior Practice Guidelines published in 2003 that includes
an updated algorithm which highlights how important airway assessment is.
Apfelbaum, Jeffrey L., Practice Guidelines for Management of the Difficult Airway: An Updated
Report by the American Society of Anesthesiologists Task Force on Management of the Difficult
Airway, Anesthesiology, 118:2 Feb 1, 2013.
Figure 1. ASA Difficult Airway Algorithm.

The purpose of the Guidelines is to facilitate the management of the

difficult airway and to reduce the likelihood of adverse outcomes [3]. If used
properly, the preanesthetic evaluation should help us figure out if the airway is
going to be difficult to manage or not and are we going to need extra resources
available to us like advanced airway devices, other anesthesia personnel in the
room to help out, all the way up to having a surgeon in the room to do an
awake tracheostomy. Also don’t forget to consider ventilation and intubation
as separate entities. Preoperatively, it is important to do a directed history and
physical. In the history, has the patient ever been told they were difficult to
ventilate or intubate and are prior operating room anesthesia records available?
Is the patient obese or do they have sleep apnea? Do they have a condition that
would predispose to difficult airway management like Downs, Treacher-
Collins or Pierre Robin syndromes, or an acute inflammatory process of the
airway or an obstructing tumor? Risk factors for difficult ventilation include,
obesity, age greater than 55 years old, history of snoring, lack of teeth,
presence of a beard, Mallampati Class three or four (See Figure 2), abnormal
mandibular protrusion test, upper airway obstruction from infection or tumor
and history of prior difficult ventilation [4]. Risk factors for difficult intubation
include long incisors, prominent over bite, interincisor distance less than 3cm,
Mallampati Class greater than 2, a high arched or narrow palate, stiff
noncompliant mandibular space, thyromental distance less than three
fingerbreadths, a short, thick neck, poor range of motion of the neck, small
mouth opening and history of prior difficult intubation [5]. The thyromental
distance is self-explanatory and basically evaluates the space available to push
the tongue in to when direct laryngoscopy is performed.
Pictorial classification of the pharyngeal structures as seen when conducting the tests.
Modified from Mallampati et al. [4, 5].
From G.L.T. Sampson, J R.B. Young, Anaesthesia, Difficult tracheal Intubation: A retrospective
Study, published Feb 22, 2007, first published May, 1987. John Wiley and Sons, Inc.. Reprinted with
permission of John Wiley and Sons, Inc.
Figure 2. Mallampati Classification.

The Mallampati Classification [6] is a way to assess mouth opening

ranging from being able to see the entire tonsillar pillars, uvula and soft palate
to not being able to see any of these structures except the hard palate, with the
implication being the less you can see the more the chance of having a difficult
time intubating the patient.
The upper lip bite test is another assessment tool we may use that assesses
jaw mobility. The patient simply tries to bring their lower teeth up over their
upper lip as far as they can go. It is not as helpful if the patient does not have
teeth. The further the patient can bring their lower teeth up over their upper lip,
the more mobile the jaw would seem to be and the easier the intubation should
be. In summary, the airway assessment is a vital component of the
preanesthetic evaluation that allows us to make appropriate plans for
management of the airway and help keep the patient safe. Also, it allows us to
talk to the patients and families about the plan, once again, discussing risks,
benefits and options so we are also staying in line with the patient’s and/or
family’s wishes.
The next several sections will deal with individual organ system elements
of the preanesthetic evaluation including the heart, lungs, and endocrine
systems. It is obviously outside the scope of this chapter to go into great detail
with regard to preanesthetic assessment, optimization and management of each
of these organ systems or all organ systems but we can certainly explore basic
concepts and relate them to how it affects decision making for the anesthetic
and entire episode of care. As we go through these next sections, remember
that timing of the procedure and available resources may affect the extent of
the assessment, optimization and management of comorbidities and should be
read in the context of the reader’s available resources. The other concept that
cannot be overemphasized is the idea that preanesthetic assessment,
optimization and management involves effective communication between
anesthesiologists, PCP’s, consultants, surgeons, proceduralists and personnel
involved in postoperative care. Most importantly, effective communication
must occur with the patient and frequently their family, caregivers or person
who is the patient’s power of attorney. Informed consent for anesthesia
involves discussing risks, benefits and options that are affected by what is
found in the preanesthetic assessment. An example would be discovering a
patient scheduled for a completely elective procedure is noted to have unstable
angina. Is the patient having anginal symptoms during the evaluation and do
they need to be evaluated by a cardiologist in an emergent fashion or can
further evaluation and management be done in a different timeframe? Does the
patient desire a workup by a cardiologist at all? Will the results of a workup
lead to management changes like what type of procedure is performed or when

it is performed? Will it change what anesthetic is used or how the patient is
monitored intra- and postoperatively? These are only some of the
considerations that must be taken into account so now let us proceed first with
cardiac evaluation.
Journal of the American College of Cardiology by American College of Cardiology. Reproduced with
permission of ELSEVIER INC. In the format Book via Copyright Clearance Center.
Figure 3. Stepwise Approach to Perioperative Cardiac Assessment.

In a review on perioperative myocardial infarction published in 2009 in

Circulation [7], Landesberg et al. stated that the 30-day mortality associated
with moderate- to high-risk noncardiac surgery in recent large cohorts and
population based studies exceeds 2% [8, 9, 10] and surpasses 5% in patients at
high cardiac risk [11], with the included citations from the review. Cardiac
complications constitute the most common cause of postoperative morbidity
and mortality [12,13], once again citing the papers included in the review.
These numbers highlight the scope of the need for perioperative cardiovascular
evaluation and strategies for management.
The 2014 ACC/AHA Guideline on Perioperative Cardiovascular
Evaluation and Management of Patients Undergoing Noncardiac Surgery was
published as a second update to the original guideline published in 1996 and
the first update published in 2007. The societies involved in this collaborative
effort in and of itself demonstrates the scope of perioperative cardiovascular
care and include the American College of Surgeons, the American Society of
Anesthesiologists, the American Society of Echocardiography, the American
Society of Nuclear Cardiology, Heart Rhythm Society, Society of
Cardiovascular Angiography and Interventions, Society of Cardiovascular
Anesthesiologists and Society of Vascular Medicine and was endorsed by the
Society of Hospital Medicine [14]. Now let’s go through the algorithm in the
updated Guidelines.
As excerpted from the Guidelines, the first step for the patient with known
CAD or patient with risk factors for CAD is to assess the urgency of the
surgery. Is the surgery an emergency? If yes then do clinical stratification as
best as possible within the time and resources available and proceed to surgery
and we do the best we can to maintain target (usually normal) heart rate, blood
pressure and oxygen saturation. If the answer is no to whether or not the case
is an emergency, the next step is to assess whether the patient is in the midst of
an acute coronary syndrome (ACS). Examples of acute coronary syndromes
include unstable angina, dangerous arrhythmias such as high grade
atrioventricular block, Mobitz 2 atrioventricular block, symptomatic
ventricular arrhythmias, supraventricular tachycardias with uncontrolled
ventricular rate, symptomatic bradycardia, or newly recognized ventricular
tachycardias. Also included would be severe valvular disease like severe or
critical aortic stenosis or symptomatic mitral stenosis. If there is an ACS the
patient should be evaluated and treated according to guideline directed medical
therapy (GDMT). If the answer is no then calculate the perioperative risk of
major adverse cardiac events (MACE). Multiple tools exist to calculate risk of
MACE including the Revised Cardiac Risk Index (RCRI) the American
College of Surgeons NSQIP calculator online, among others. If the patient has
a low risk of MACE meaning less than 1%, proceed to surgery with no further
testing. If the estimated risk is greater than 1%, then determine the functional
capacity of the patient. If the patient has moderate, good or excellent
functional capacity, meaning greater than 4 metabolic equivalents (MET’s)
(See Figure 4) then proceed to surgery with no further testing. If the patient
has poor or unknown functional capacity, the clinician should consult with the
patient and perioperative team to determine if further testing would impact
patient decision making regarding the original surgery or procedures resulting
from further testing. If the answer is no then proceed to surgery according to
GDMT or alternate strategies such as noninvasive treatment of the indication
for surgery. If the answer is yes, stress testing may be appropriate. If stress
testing is normal then the patient would proceed to surgery according to
GDMT or alternate strategies such as noninvasive treatment of the indication
for surgery. If stress testing is abnormal then the patient would proceed to
coronary revascularization according to existing clinical practice guidelines
(CPG’s). Once again, this entire paragraph is excerpted from the Guidelines.
The paper should be read in its entirety for more in depth coverage on each
step in the algorithm [15].
Reprinted from Mayo Clinic Proceedings Volume 72:6, Kim A. Eagle, Bruce H. Brundage, Bernard R.
Chaitman, Gordon A. Ewv, Lee A. Fleisher, Norman R. Hertzer, Jeffrey A. Leppo, Thtomas Ryan,
Robert C. Schlant, William H. Spencer, John A. Spittell, Richard D. Twiss, Guidelines for
Perioperative Cardiovascular Evaluation for Noncardiac Surgery: An Abridged Version of the Report
of The American College of Cardiology/American Heart Association Task Force on Practice
Guidelines. 524-531, June 1997, with permission from ELSEVIER.
Figure 4. Metabolic Equivalents.
There is much more to the Guidelines than just the algorithm but out of
the scope of this chapter so we will move on to one other aspect of
preoperative cardiovascular care involving cardiovascular implantable
electronic devices (CIED’s). In 2011, The Heart Rhythm Society/American
Society of Anesthesiologists Expert Consensus Statement on the Perioperative
Management of Patients with Implantable Defibrillators, Pacemakers and

Arrhythmia Monitors: Facilities and Patient Management document was
published. In it, preoperative recommendations are made that include the
CIED management team, as well as the anesthesiologist, surgeon and others
taking care of the patient perioperatively.
Tables 3 and 4 highlight essential elements of the information required by
the CIED team as well as the perioperative care team as well as preoperative
recommendations (Table 2) [16].
Table 2. Preoperative recommendations
Reprinted from Heart Rhythm, Volume 8, George H. Crossley, Jeanne E. Poole, Marc A. Rozner,
Samuel J. Asirvatham, Alan Cheng, Mina K. Chung, T. Bruce Ferguson, John D. Gallagher, Michael L.
Gold, Robert H. Hoyt, Samuel Irefin, Fred M. Kusumoto, Liza Prudente Moorman, Annemarie
Thompson, The Heart Rhythm Society(HRS)/American Society of Anesthesiologists(ASA) Expert
consensu Statement on the Perioperative Management of PAtients with Implantable Defibrillators,
Pacemakers and Arrhythmia Monitors:Facilities and PAtient Management. This document was
developed as a joint Project with the American Society of Anesthesioloigsts(ASA), and in collaboration
with the American Heart Association(AHA), and the Society of thoracic Surgeons(STS).1114-1154,
July 2011, July 2011, with permission of ELSEVIER.
Communication is clearly key in the safe perioperative management of

patients with these devices that is done in an interdisciplinary fashion. Now let
us move on to the pulmonary system.
Preoperative assessment of the lungs should focus first on identification of
new or preexisting disease, treatment regimens and physical exam. Also, is the
patient optimized and if not, do we have time to optimize them? What are we
concerned about preventing in the first place? Postoperative pulmonary
complications can be defined in many ways but most would consider them to
be clinically significant atelectasis, pneumonia, respiratory failure and
exacerbation of underlying chronic lung disease [17]. Anesthesiologists may
also be concerned about the risk of bronchospasm or laryngospasm during the

conductance of an anesthetic. Patient related risk factors for postoperative
pulmonary complications include chronic obstructive pulmonary disease, age
greater than 60 years, ASA class 2 or greater, functional dependence and a
history of congestive heart failure and patients with a low serum albumin level
[18]. Procedure related factors include aortic thoracic or abdominal (especially
upper) surgery, neurosurgery, head and neck surgery, emergency surgery,
prolonged surgery and general anesthesia [19]. There are multiple pulmonary
risk calculators available (two cited) to help discuss risk with patients and to
help guide clinical decision making as it relates to the procedure and the
anesthetic [20, 21].
Table 3. Essential elements of the information given to

the CIED physician
Table 4. Essential elements of the preoperative CIED evaluation to be

provided to the operative team
From the ACP Guidelines, preoperative risk reduction strategies include

lung expansion modalities such as incentive spirometry, chest physical
therapy, deep breathing exercises, cough, postural drainage, percussion and
vibration, suctioning and ambulation, intermittent positive-pressure breathing
and continuous positive-airway pressure [22]. Additionally, it seems
reasonable to delay surgery if possible to treat underlying pulmonary infection

and also to optimize airflow for patients with obstructive disease with
medications if the patient is not optimized. Once again, communication with
the patient’s PCP, pulmonologist and surgeon is important for optimization if
timing of the surgery permits it. As far as smoking and smoking cessation
goes, it is clear we should recommend that patients stop smoking for as long as
possible both before and after surgery, and patients should obtain help in doing
so [23]. There still seems to be some debate in the literature about optimal
timing of cessation prior to surgery but from a review and meta analysis by
Wong et al. published in 2012, their conclusions were that stopping smoking at
least four weeks in advance reduces respiratory complications and that
abstinence for less than four weeks does not appear to affect risk of
postoperative complications [24].
Let us look briefly now at endocrine disorders, primarily diabetes. Patients
with and without diabetes with perioperative hyperglycemia over a variety of
procedures have increased length of stay, hospital complications and mortality
after surgery [25, 26]. During the preanesthetic evaluation, the history and
physical should include how long the patient has had diabetes and how well
controlled it is. Have there been complications associated with diabetes like
cardiovascular disease, renal disease, or neuropathy to name a few. Has the
patient ever been admitted for diabetic ketoacidosis or other complications
from diabetes? Does the patient have a recent hemoglobin A1c and/or a
random or fasting glucose? At what blood glucose level does the patient feel
bad (hypo- and hyperglycemia)? Does the patient have an endocrinologist or
PCP that manages the patient’s glucose? Does the patient have an insulin
pump? As far as management goes, let’s talk philosophically about
preoperative blood glucose management. If the patient is poorly controlled,
communication must take place with the surgeon, the patient and those
involved in the patient’s care to see if the procedure can be postponed until the
patient is under better control. If not, endocrinology may be consulted and
would proceed when the surgeon, anesthesiologist, patient and family are all in
agreement about optimal timing. If the patient is under acceptable control, it is
clearly desirable to avoid hypoglycemia as well as keeping their blood sugar
under reasonable control, which may be defined differently for different
patients.
In patients with thyroid disease, whether it be hypo- or hyperthyroidism,
are they symptomatic? What is their treatment regimen? The goal is for
patients to be euthyroid so as to avoid myxedema coma with hypothyroidism
and thyroid storm in patients with hyperthyroidism. As previously mentioned,
communication with the patients PCP or endocrinologist is critical, especially

if the patient requires a time sensitive, urgent or emergent procedure and if the
patient has no PCP or endocrinologist an endocrine consult should be
obtained. If the procedure is elective then it should be postponed until the
patient is euthyroid. There are many more endocrine conditions that patients
present with either as a comorbid condition or as the reason for a procedure
that go beyond the scope of this chapter so let us proceed on to preoperative
medication management.
Medication management in the perioperative period can be complex and is
not always guided by high level evidence or high class recommendations in
relation to benefit and risk. What medications should be held in the days
leading up to surgery or the day of surgery? Which medications can be or
should be continued even the day of surgery? When should medications be
restarted postoperatively? As with the rest of the preoperative evaluation,
information gathering is where to start. Especially for medications, this
frequently is more difficult than it sounds. Hopefully the patient has a
complete list of their medications as well as medication or other allergies. If
this is not the case, medication reconciliation with the patient’s PCP or
pharmacy is a good next step if time and resources permit. Even then, what the
patient is prescribed and what the patient takes on a regular basis may differ so
going over any list obtained with the patient or caregiver is important.
Preoperative medication management needs to be personalized for each
patient, weighing risks and benefits of continuing versus stopping medications
in the context of the comorbid conditions being treated by the medications as
well as the impact of continuing versus stopping on the procedure or the
patient’s postoperative course. For instance, from the ACC/AHA Guidelines,
there is a Class 1 recommendation (benefit far outweighs risk) with level B
evidence stating beta blockers should be continued in patients undergoing
surgery who have been on beta blockers chronically and the same is true for
statins [27]. With that in mind, perioperative medication management should
certainly be influenced very strongly by a deep knowledge of national
guidelines when available, but ultimately need to be tailored to individual
patients and the procedure being performed. It is valuable to explore what
recommendations exist at your individual institution, how they were derived
and how they apply to your individual patients. Discussion amongst providers,
patients, surgeons, and anesthesiologists is critical to maximizing the benefit
and minimizing the risk as best as possible while working within the wishes of
the patient.
Testing in the preoperative period should be dictated by what is

discovered on the history and physical, highlighting comorbidities and the
character of the procedure. Testing should be selective and not routine [28].
ECG, chest radiographs, lab testing for hemoglobin, hematocrit, coagulation
studies, electrolytes or even pregnancy testing all should be done for
indications specific to the patient or the procedure, especially when the results
of a test or tests influence the need for further testing or will have an effect on
perioperative management. For instance, a young woman scheduled for a time
sensitive procedure is found to be pregnant. That data would have a profound
influence on the discussion about risks, benefits and options for the procedure
in regard to the mother and now the fetus. This information may also strongly
influence timing of the procedure as well as monitoring pre-, intra- and
postoperatively. Another example of preoperative testing influencing the
episode of care would be a patient at risk for being anemic who is found to be
anemic prior to an elective procedure. This patient may now require
optimization so that we are maximizing benefit and minimizing risk as best we
can.
The future holds many opportunities to improve preanesthetic evaluation
as it relates to identification, optimization and management of conditions for
which patients are having surgery as well as comorbid conditions. Are there
better ways to assess, optimize, monitor and manage patients with Alzheimer’s
disease or other dementias? How long should a diabetic patient be under better
glucose control prior to a procedure and what is the glucose target for an
individual patient? How will we manage medications built for an individual
patient based on their genome? How will information technology affect
preoperative information gathering as well as transmission of that data
downstream through the entire perioperative episode of care and then allowing
us to look at outcome data to influence upstream processes back in the
preanesthetic evaluation? These are only a few of many questions to be looked
at in the future
REFERENCES
[1] Apfelbaum JL, Connis RT, Nickinovich DG. Practice Advisory for
Preanesthetic Evaluation, Anesthesiology, 2012; 116: No 3 1-1.
[3] Apfelbaum JL, Hagberg CA, Caplan RA, Blitt CD, Connis RT,
Nickinovich DG, Practice Guidelines for Management of the Difficult
Airway, Anesthesiology, V 118 No 2, 2013.
[4] El-Orbany, Woehick HJ, Difficult Mask Ventilation. Anesthesia and
Analgesia, vol. 109, Issue 6, pp. 1870-1880df.
[5] Apfelbaum JL, Hagberg CA, Caplan RA, Blitt CD, Connis RT,
Nickinovich DG Practice Guidelines for Management of the Difficult
Airway, Anesthesiology, V 118 No 2, 2013. Apfelbaum JL, Connis RT,
Nickinovich DG.
[6] Mallampati RS, Gatt, SP, Gugino LD, Desai SP, Waraksa B, Freiberger
D, Liu, PL. A Clinical Sign to Predict Difficult Tracheal Intubation: A
Prospective Study. Canadian Anaesthetists’ Society Journal,1985 32:4
pp 429-434.
[7] Landesberg G, MD, DSc; Beattie, WS MD, PhD; Morris Mosseri M,
MD; Jaffe AS, MD; Alpert JS, MD. Periperative Myocardial Infarction.
Circulation 2009; 119:2936-2944.
[8] Lindenauer PK, Pekow P, Wang K, Mamidi DK, Gutierrez B, Benjamin
EM. Perioperative beta-blocker therapy and mortality after major
noncardiac surgery. N. Engl. J. Med. 2005;353:349-361.
[9] Wu WC, Schifftner TL, Henderson WG, Eaton CB, Poses RM, Uttley G,
Sharma SC, Vezeridis M, Khuri SF, Friedmann PD. Preoperative
hematocrit levels and postoperative outcomes in older patients
undergoing noncardiac surgery. JAMA. 2007;297:2481-2488.
[10] Lee TH, Marcantonio ER, Mangione CM, Thomas EJ, Polanczyk CA,
Cook EF, Sugarbaker DJ, Donaldson MC, Poss R, Ho KK, Ludwig LE,
Pedan A, Goldman L. Derivation and prospective validation of a simple
index for prediction of cardiac risk of major non-cardiac surgery.
Circulation. 1999;100:1043-1049.
[11] Fleisher LA, Eagle KA, Shaffer T, Anderson GF. Perioperative- and
long-term mortality rates after major vascular surgery: the relationship to
preoperative testing in the medicare population. Anesth. Analg.
1999;89:849-855.
[12] Lee TH, Marcantonio ER, Mangione CM, Thomas EJ, Polanczyk CA,
Cook EF, Sugarbaker DJ, Donaldson MC, Poss R, Ho KK, Ludwig LE,
Pedan A, Goldman L. Derivation and prospective validation of a simple
index for prediction of cardiac risk of major non-cardiac surgery.
Circulation. 1999;100:1043-1049.
[13] POISE Study Group. Effects of extended-release metoprolol succinate in

patients undergoing non-cardiac surgery (POISE trial): a randomized
controlled trial. Lancet. 2008;371:1839-1847.
[14] Fleisher LA, Fleischmann KE, Auerbach AD, Barnason SA, Beckman
JA, Bozkurt B, Davila-Roman VG, Gerhard-Herman MD, Holly TA,
Kane GC, Marine JE, Nelson MT, Spencer CC, Thompson A, Ting HH,
Uretsky BF, Wijeysundera DN. 2014 ACC/AHA guideline on
perioperative cardiovascular evaluation and management of patients
undergoing noncardiac surgery: a report of the American College of
Cardiology/American Heart Association Task Force on Practice
Guidelines. Circulation. 2014;130:e278-e333.
[16] Crossley GH, Poole JE, Rozner MA, Asirvatham SJ, ChengA, Chung
MK, Ferguson TB Jr., Gallagher JD, Gold MR, Hoyt RH, Irefin S,
Kusumoto FM, Moorman LP, Thompson A. The Heart Rhythm
Society/American Society of Anesthesiologists Expert Consensus
Statement on the Perioperative Management of Patients with
Implantable Defibrillators, Pacemakers and Arrhythmia Monitors:
Facilities and Patient Management. Heart Rhythm 2011;8:1114-1152.
[17] Qaseem A, Snow, V, Fitteman N, Hornbake R, Lawrence VA, Smetana
GW, Weiss K, Owens DK. Risk Assessment for and Strategies to
Reduce Perioperative Pulmonary Complications for Patients Undergoing
Noncardiothoracic Surgery: A guideline from the American College of
Physicians. Ann. Intern. Med. 2006;144(8):575-580.

[20] Gupta H, Gupta PK, Fang X, Miller WJ, Cemaj S, Forsse RA, Morrow
LE. Development and validation of a risk calculator predicting
postoperative respiratory failure. Chest 2011 Nov;140(5):1207-15.
[21] Arozullah AM, Daley J, Henderson HG, Khuri SF. Multifactorial Risk
Index for Predicting Postoperative respiratory Failure in Men after
Major Noncardiac Surgery. Annals of Surgery. Vol. 232, No. 2, 2000,
242-253.
[23] American Society of Anesthesioloigsts House of Delegates Statement on
Smoking Cessation. Approved by the ASA House of Delegates October
22, 2008.
[24] Wong J, Lam DP, Abrishami A, Chan MTV, Chung F. Short-term
preoperative smoking cessation and postoperative complications: a
systematic review and mate-analysis. Canadian Journal of Anesthesia.
(2012) 59;268-279.
[25] Frisch A, Chandra P, Smiley D, Ping, Rizzo M, Gatcliffe C, Hudson M,
Mendoza J, Johnson R, BS, Lin E, and Umpierrez GE. Prevalence and
Clinical Outcome of Hyperglycemia in the Perioperative Period in
Noncardiac Surgery. Diabetes Care, 2010 Aug; 33(8): 1783-1788.
[26] Gandhi GY, Nuttall GA, Abel MD, Mullany CJ, Schaff HV, Williams
BA, Schrader LM, Rizza RA, McMahon MM. Intraoperative
Hyperglycemia and Perioperative Outcomes in Cardiac Surgery Patients.
Mayo Clinic Proceedings. July 2005, Volume 80, Issue 7, pp. 862-866.
Chapter 3
ANESTHETIC DRUGS FOR

THE NON-ANESTHESIOLOGIST
Jeffrey Oldham, MD
Department of Anesthesiology, University of Kentucky
College of Medicine, Lexington, Kentucky, US
ABSTRACT
The goal of anesthesia is to obtain a combination of amnesia,
analgesia and muscle relaxation in order to facilitate surgical procedures.
Unfortunately, no single drug can accomplish all of these goals. Instead, a
combination of different drugs must be utilized in order to achieve a
balanced and effective anesthetic. These drug combinations may be
tailored to meet individual surgical and patient needs. Of the commonly
used anesthetic drugs, there are several major classes including induction
drugs, inhalational agents, opioids and paralytics. These broad classes
will be the focus of this chapter.
INDUCTION DRUGS
Propofol
Propofol is one of the most commonly administered induction agents in

modern anesthetic practice. It is an alkyl phenol used for its hypnotic
24 Jeffrey Oldham
properties [1]. Propofol is insoluble in water and therefore must be formulated

with a combination of lipids including soybean oil, glycerol and purified egg
phosphatide [2]. Because of the lipid component, propofol is very conducive
to bacterial growth and unused medication should be discarded within six
hours of first use.
Propofol binds to -aminobutyric acid (GABA) receptors and causes an
inhibitory influx of chloride ions. This drug has an expedient onset of action
with peak effect following standard induction dose of 2 mg/kg occurring at
roughly ninety seconds. Effect from single bolus dosing may last 5-10 minutes
and termination of action is largely due to redistribution of the drug to
peripheral tissue. Metabolism of propofol occurs in the liver with no known
active byproducts.
The benefits of propofol include rapid onset, rapid termination of action
from single bolus dose, and superb blockade of upper airway reflexes required
during laryngoscopy. The main disadvantage of propofol is a significant
decrease in systemic vascular resistance causing hypotension. The hypotension
can be quite severe with an estimated 25-40% reduction in systolic blood
pressure following an induction dose [2].
Caution should be used in patients with coronary artery disease and
cerebrovascular disease as the reduction in blood pressure may compromise
both coronary and cerebral perfusion. Induction agents with less labile
cardiovascular effects should be considered in this patient population. Concern
has also been raised in patients with a documented food allergy to eggs but this
does not appear to have a correlation with allergic reaction to propofol.
Propofol is particularly useful when run as an infusion for total
intravenous anesthesia (TIVA) and is commonly combined with short acting
narcotic infusions such as remifentanil when inhalational agents are
contraindicated (patients with severe postoperative nausea/vomiting and
surgical procedures requiring somatosensory evoked potential or motor evoked
potential monitoring). Propofol infusion is also frequently utilized in the
intensive care unit for sedation in mechanically ventilated patients. Prolonged
administration of propofol infusions must be used cautiously as this has been
associated with propofol infusion syndrome – a rare clinical condition
characterized by profound bradycardia, metabolic acidosis, rhabdomyolysis,
hyperlipidemia and enlarged or fatty liver [2].
Anesthetic Drugs for the Non-Anesthesiologist 25
Etomidate
Etomidate is a carboxylated imidazole-containing compound that is

structurally unique when compared to other classes of intravenous induction
agents. This drug is formulated with propylene glycol in order to maintain
stability in aqueous solution.
Similar to propofol, the mechanism of action is believed to involve
inhibition of GABA receptors resulting in hypnosis. Standard induction dosing
of etomidate is 0.2-0.3 mg/kg. Onset of hypnosis is rapid with duration of
action lasting 200-300 seconds [3]. Metabolism of etomidate occurs in the
liver with no active byproducts.
The most pronounced benefit of etomidate is hemodynamic stability
following induction dosing. Unlike propofol, etomidate does not cause a
significant drop in blood pressure which makes it an appropriate choice in
hemodynamically unstable patients or in those who are at risk for comprised
coronary or cerebral perfusion with hypotension (i.e., patients with coronary
artery disease or carotid stenosis). Disadvantages to etomidate include
increased incidence of postoperative nausea/vomiting as well as adrenal
suppression. Adrenal suppression occurs through inhibition of cortisol
synthesis. Research in this area has shown increased mortality in ICU patients
receiving etomidate infusion for sedation, but even single bolus dosing may
suppress cortisol synthesis for 5-8 hours [4]. Recent evidence even shows
increased morbidity and mortality after a single dose [9]. Etomidate should be
used in caution in patients with seizure disorder as it may enhance epileptiform
active.
Ketamine
Ketamine is structurally similar to phencyclidine (the recreational drug

PCP, used for its hallucinogenic properties) that produces a dissociative
anesthetic state consisting of both unconsciousness and analgesia. The
mechanism of action involves antagonism of the NMDA receptor. There also
appears to be some activity at opioid receptors in the brain and spinal cord [2].
Induction doses of ketamine range from 1-2 mg/kg IV (4-8 mg/kg IM).
This results in rapid onset of anesthesia with duration of action lasting 10-20
minutes [5]. Metabolism occurs in the liver resulting in the active metabolite
norketamine (20-30% activity of ketamine) which then undergoes renal
elimination [2].
26 Jeffrey Oldham
The cardiovascular effects of ketamine are very different from other

intravenous anesthetic agents. Unlike other anesthetic agents which tend to
cause reduction or no change in blood pressure, ketamine actually causes an
increase in systemic vascular resistance, heart rate and cardiac output. The
mechanism behind this property may be related to stimulation of the
sympathetic nervous system and endogenous release of norepinephrine. It is
important to note, however, that ketamine is a negative inotrope which may
cause a reduction in cardiac contractile strength [2]. Though the negative
inotropy is typically overcome by the augmentation of heart rate and systemic
vascular resistance, critically ill patients may not be able to compensate for the
myocardial depressant effect. In light of these properties, ketamine is
frequently used for induction of hemodynamically unstable trauma patients to
avoid the disastrous hemodynamic effects of decreasing systemic vascular
resistance in a patient with significant blood loss. Ketamine should be avoided
in patients with severe coronary artery disease as the increase in systemic
vascular resistance and heart rate will increase myocardial oxygen demand and
may predispose the patient to ischemia.
Another unique property of ketamine is its ability to augment cerebral
metabolic oxygen consumption, cerebral blood flow and intracranial pressure.
Because of this, ketamine should be avoided in patients with poor intracranial
compliance. Although concern has been raised over the use of ketamine in
patients with seizure disorders, it is generally accepted that ketamine does not
induce seizures and may actually be used as an anti-epileptic.
Ketamine also has several unique respiratory effects that can be useful
during anesthesia. These include maintenance of spontaneous ventilation and
some upper airway reflexes as well as bronchodilation. The maintenance of
spontaneous ventilation and intact upper airway reflexes should not, however,
obviate the need for endotracheal intubation in patients at risk for aspiration.
In addition to its use as an induction agent, ketamine may also be used in
low doses as an analgesic or for short procedures requiring conscious sedation
(reduction of a fracture in the emergency department or bedside wound care).
It has also been used as an infusion to treat depression.
Midazolam
Midazolam is a short acting benzodiazepine frequently used for anxiolysis

prior to induction of anesthesia. Like all benzodiazepine drugs, midazolam
provides anterograde amnestic, sedative, anticonvulsant and muscle relaxant
properties in addition to anxiolysis. Mechanism of action involves binding to

GABA receptors as was discussed with both propofol and etomidate. The
primary adverse effect of midazolam is respiratory depression which may be
worsened by coadministration with narcotics.
Athough midazolam has historical significance as an induction agent,
current practice utilized it for preoperative sedation. Typical dosing for
midazolam as premedication to reduce anxiety prior to arrival in the operating
room is .04-.08 mg/kg IV. Children without IV access frequently require 0.5
mg/kg PO approximately 15 minutes prior to the operating room. Preoperative
administration of versed must be used cautiously, however, as the sedative
effects may prolong emergence from anesthesia or cause postoperative
cognitive dysfunction that might limit one’s ability to complete an accurate
neurologic exam. Midazolam may also be used for sedation during relatively
noninvasive procedures such as central line placement, epidural placement,
peripheral nerve block, etc. Additionally, versed may be given as an infusion
for sedation in mechanically ventilated ICU patients.
Metabolism of versed takes place via oxidation-reduction reactions in the
liver. The metabolite produced during its metabolism, -hydroxymidazolam,
is much less potent than midazolam but may accumulate with prolonged
infusion. Other commonly used benzodiazepines include diazepam
(intermediate duration of action) and lorazepam (long duration of action).
Discussion of benzodiazepines would not be complete without reviewing
flumazenil, a competitive antagonist that binds GABA receptors with high
affinity but possesses minimal intrinsic activity. Flumazenil is given to reverse
the effects of benzodiazepines and may require repeated dosing or continuous
infusion to provide antagonism until the benzodiazepine has been fully
metabolized.
INHALATIONAL AGENTS
Fortunately for modern day patients and physicians, inhalational based
anesthetics have certainly come a long way since the introduction of nitrous
oxide and diethyl ether. The three most commonly used modern anesthetic
gases include desflurane, sevoflurane and isoflurane. The discussion of
inhalational anesthetics will begin with a generalized overview followed by
specific characteristics of each inhalational agent.
Inhalational anesthetic agents are unique in that the mechanism of action
is unclear. One leading hypothesis involves the interaction of inhalational
28 Jeffrey Oldham
anesthetics with neurotransmitter gated ion channels such as GABA, glycine

and NMDA-type glutamate receptors [10]. These agents are most frequently
discussed in terms of their minimum alveolar concentration (MAC) which is
the percent of inhaled agent required in the lung alveolus to prevent movement
following surgical incision in 50% of patients. Therefore, MAC can be viewed
as a measure of anesthetic potency with agents having a lower MAC being
more potent than those having a higher MAC. Potency appears to be correlated
with lipid solubility as those agents with higher lipid solubility have a lower
MAC.
These inhalational agents are delivered through an anesthesia breathing
circuit from special devices called vaporizers that are agent-specific and
calibrated to accurately and precisely deliver the agent in vapor form.
Inhalational agents are delivered to the alveolus through either
spontaneous inhalation or mechanical ventilation. The agent then diffuses
down its concentration gradient into the alveolar capillaries where it is
transported to systemic tissue (most notably the brain). The reverse effect
occurs once delivery of the inhalational agent to the lungs is ceased –
inhalational agent is transported from the peripheral tissues back to the lungs
via the blood where it is then exhaled. Minimal metabolism of inhalational
agents occurs.
The most common adverse effect from inhalational agents proves to be a
decrease in systemic vascular resistance resulting in hypotension. This is
commonly compounded by the fasting state required before surgery which
provides for a relatively hypovolemic patient. The hypotension can be
ameliorated with judicious intravenous fluid replacement and vasoactive
medications such as phenylephrine.
Desflurane is an inhalational agent with a MAC of approximately 6%. It
has the lowest lipid solubility of the three most commonly used inhalational
agents, and therefore, has a higher MAC. Due to its low lipid solubility, there
is minimal uptake by peripheral tissues which allows for a very “fast on” and
‘fast off” effect. Of note, rapid escalation of the concentration of desflurane
has been found to elicit a sympathetic response resulting in tachycardia and
hypertension. Because of this, it is best to slowly raise the concentration of
desflurane delivered to a patient until the desired level of anesthesia is
reached.
Sevoflurane has an intermediate lipid solubility with a resulting MAC of
approximately 2%. Sevoflurane is unique because unlike desflurane and
isoflurane, inhalation of this gas is not irritating to the airway. This feature
allows sevoflurane to be used for inhalational induction of anesthesia.
Inhalational induction of anesthesia occurs when the patient breathes a mixture

of sevoflurane and oxygen through the anesthesia breathing circuit until
unconsciousness is achieved. Such an induction is useful in children who lack
intravenous access as well as in patients who require the maintenance of
spontaneous ventilation (the majority of intravenous anesthetic drugs cause
apnea with bolus dosing). Also unique to sevoflurane, is the potential by-
product known as “compound A” which was found in animal studies to be
nephrotoxic, although this has not been corroborated in human trials.
Isoflurane is the final agent to be discussed in this review. Of the agents
listed above, isoflurane is the most potent with a MAC of approximately 1%.
Because of the high lipid solubility of this gas, there can be considerable
uptake by peripheral tissues which can impede recovery from the anesthetic
following cessation of gas delivery. Care must be taken to discontinue
isoflurane administration earlier than the other inhalational agents when
planning for wake-up from an anesthetic.
It is important to note that these gases are very complex agents that should
never be used by unqualified personnel. Due to the reduction in systemic
vascular resistance and cardiodepressant effects, potential cardiovascular
collapse requires careful monitoring of the inspired and expired concentrations
as well as careful calibration and maintenance of the gas delivery systems.
Additionally, expertise in airway management is essential in the safe
administration of inhalational anesthetic agents.
Opioids
Opioids have long been a mainstay in the treatment of pain both inside
and outside of the operating room. Though differing in potency as well as
duration of action, all narcotics work via agonism of opioid receptors (mu,
kappa and delta subtypes) in the central nervous system, peripheral nervous
system and even peripheral tissues. Although they do provide profound
analgesia, numerous side effects exist including, but not limited to, sedation,
respiratory depression, hypotension, constipation, urinary retention, itching
and tolerance to analgesic effect. Because of tolerance, escalating doses of
opioids are required in chronic pain conditions.
Fentanyl is one of the most commonly used opioids in current anesthetic
practice. Its fast onset time and relatively short duration of action make it an
appropriate choice to treat surgical stimulation which frequently has waxing
and waning periods of intensity. Fentanyl is used during induction of
30 Jeffrey Oldham
anesthesia at doses of 2-6 mcg/kg IV [6] to blunt the sympathetic response to

direct laryngoscopy as well as for pain control both during and after surgery.
Typical dosing in an adult ranges from 50-100 mcg IV. Of note, fentanyl is
available in IV formulation, transdermal patch and oral “lollipops” (used only
in chronic pain situations). It may also be administered intranasally.
Unfortunately, its use as a street drug is increasing, and its potency is such that
overdosing and death is much more common than with other street drugs.
Morphine is another frequently utilized narcotic by anesthesiologists. It is
the prototypical opioid against which all other opioids are compared (see table
below for comparison of potencies). With a slower time to peak effect and
longer duration of action than fentanyl, morphine is frequently used prior to
emergence from anesthesia to provide for pain control during the transition to
the recovery room. Additionally, morphine is a commonly used analgesic in
the recovery room. Typical adult dosing ranges from 4-8 mg IV. Morphine
must be used cautiously in patients with renal insufficiency because the active
metabolite Morphine-6-glucuronide is renally excreted and may cause
significant sedation and respiratory depression. Also of note is the potential
histamine release associated with morphine administration which may cause
hypotension with intravenous dosing.
Hydromorphone is another anesthetic staple in the armamentarium of
medications used to treat perioperative pain. Hydromorphone is similar to
morphine in its time of onset and duration of action but is not associated with
the histamine release common with morphine administration. Also like
morphine, hydromorphone is most frequently used for pain control in the
recovery room.
Sufentanil is the most potent narcotic utilized in anesthetic practice with
clinical potency ratio 2,000 to 4,000 times that of morphine and 10 to 15 times
that of fentanyl [7]. Sufentanil may be given as an IV bolus with similar
pharmacokinetics as fentanyl but is more frequently utilized as a continuous
infusion during anesthesia. Specific information regarding continuous infusion
of opioids will be discussed in a later section.
Remifentanil is a unique opioid secondary to its metabolism by ester
hydrolysis. Unlike previously discussed opioids, remifentanil metabolism is
unaffected by hepatic or renal insufficiency. Additionally, the unique
metabolic pathway allows for very expedient recovery from drug effect. The
short duration of action makes remifentanil a perfect choice for continuous
infusion during total intravenous anesthetic techniques. Because both
remifentanil and sufentanil are extremely potent narcotics, their use should be
limited to those specifically trained in their administration who have expertise
in airway management as there is a very small margin of error in regard to

respiratory depressant effects and potential cardiovascular collapse.
Demerol is another commonly used narcotic in the perioperative period. It
is unique in the way it provides more of a euphoric effect than other similar
drugs. Additionally, it may be given to reduce the discomfort of postoperative
shivering that may occur in the PACU. Caution must be used in patients with
seizures as the major metabolite of this drug, normeperidine, may reduce
seizure threshold in susceptible patients.
One cannot have a complete discussion of opioids without addressing
continuous infusion of narcotics. Unlike single bolus dosing, the clearance of
narcotics following a continuous infusion is highly dependent on the drug
chosen as well as the duration of the infusion. The pharmacokinetics of
continuous narcotic infusions is best described by the context-sensitive half-
time which is defined as the time required to achieve a 50% decrease in
concentration after stopping a continuous, steady-state infusion [8]. For most
opioids, the longer the drug is infused, the longer it will take to be metabolized
following cessation of the infusion. Some drugs such as morphine and fentanyl
have surprisingly long time periods required for metabolism following such an
infusion compared to sufentanil and remifentanil.
NEUROMUSCULAR BLOCKADE
Surgical procedures frequently require an immobile patient. Although
inhalational agents combined with intravenous agents such as narcotics and
sedatives can provide for an immobile patient, the careful administration and
monitoring of a paralyzing agent can help improve the margin of safety when
immobility is required for safe surgical intervention.
In order to understand the paralysis induced during anesthesia, one must
first understand the chain of events that causes skeletal muscle contraction. A
pre-junctional nerve fiber carries an electrical signal down its path until it
reaches the end of the nerve. At this point, an influx of calcium ions causes the
release of acetylcholine (ACh) from the nerve terminal into the synaptic cleft
between the pre-junctional and post-junctional nerve fibers. The ACh then
diffuses across the synaptic cleft and binds ACh-receptors on the post-synaptic
nerve. Binding of the ACh molecule to the post-synaptic nerve fiber then
causes a change in membrane permeability allowing for a depolarization of the
post-synaptic motor nerve fiber. This depolarization is then transferred along
the post-synaptic nerve fiber and is propagated to the muscle fiber resulting in
32 Jeffrey Oldham
contraction. The ACh is metabolized by acetylcholinesterase enzymes

concentrated heavily in the synaptic cleft.
Blockade of this signal transmission may be achieved with administration
of neuromuscular blocking drugs (NMBs). These drugs are subdivided into
depolarizing and non-depolarizing neuromuscular blocking drugs. These will
be further discussed below.
Depolarizing NMBs – succinylcholine is the only depolarizing
neuromuscular blocking drug. It acts as a competitive agonist by mimicking
ACh at the ACh receptor on the post-junctional membrane. Succinylcholine
binds to the ACh receptor and causes a depolarization just as ACh would.
Unlike ACh, succinylcholine causes a sustained depolarization which
ultimately renders the receptor inactive. The depolarization is visualized on the
patient as skeletal muscle fasciculation (short-lived contraction of the muscles)
following administration of the drug. Succinylcholine is metabolized by
plasma cholinesterase (pseudocholinesterase) which is a different enzyme than
acetylcholinesterase.
Succinylcholine is unique in its speed of onset and short duration of
action. An intubating dose of 1 mg/kg IV takes effect in 30-60 seconds with
recovery of muscular function in 5-10 minutes. Such rapidity makes it ideal of
emergency control of the airway.
Contraindications to the use of succinylcholine are related to the drug’s
ability to raise extracellular potassium levels. Plasma potassium can be raised
by approximately 0.5 mEq/L in normal patients following administration of
succinylcholine. Patients at risk for an exaggerated and potentially lethal rise
in potassium include those with an upregulation of ACh-receptor density in
areas outside of the neuromuscular junction. This includes patients who have
suffered large burns, spinal cord injuries, stroke patients with residual motor
deficits, and children with neuromuscular disorders such as Duchenne
muscular dystrophy. Because of cases of cardiac arrest in children with
undiagnosed muscular dystrophy following succinylcholine administration, the
drug is not commonly used in children unless required for emergency control
of the airway.
Non-depolarizing NMBs – commonly used drugs in this category include
rocuronium, vecuronium and cisatracurium. All of these drugs work by
binding the ACh-receptor on the post-junctional membrane and preventing ion
influx thus blocking any signal transduction along the motor nerve to the
muscle fiber. Since depolarization is blocked with these drugs, there is no
visible muscle contraction following administration as is seen with
succinylcholine. These drugs have a longer onset of action, but administration
of large doses of rocuronium (1.2 mg/kg) may approximate the speed of

succinylcholine. Both rocuronium and vecuronium undergo primary hepatic
metabolism though there is significant contribution from renal elimination.
Cisatracurium, however, undergoes a unique breakdown known as Hoffman
elimination that is independent of hepatic or renal function. Such unique
metabolism makes cisatracurium a frequent choice for neuromuscular
blockade in patients with renal failure.
The level of paralysis is monitored using electrical nerve stimulation. By
applying a nerve stimulator to a peripheral nerve (frequently the ulnar nerve or
branches of the facial nerve) one is able to follow the effect of neuromuscular
blockade. This is most commonly monitored via a train-of-four (TOF)
stimulation which involves four fast electrical impulses delivered to the nerve.
Non-depolarizing NMB will slowly recover muscular function as evidenced
by one twitch (visible muscle contraction) as the drugs are metabolized. As
more and more drug is degraded, additional twitches will be noted until all
four electrical stimulations result in a muscular twitch. Succinylcholine, on the
other hand, has more of an “on and off” effect where there are no twitch
responses to electrical stimulation while the drug is active with a prompt return
of four twitches after it is metabolized. Monitoring the TOF allows the
anesthesiologist to assess the level of neuromuscular blockade and assist in
deciding when to redose NMB agents.
Reversal of neuromuscular blockade is a fairly complicated topic but will
be approached in the most straight-forward manner possible for this
discussion. Succinylcholine does not require reversal prior to extubation as it
is metabolized expediently by pseudocholinesterase. Non-depolarizing
NBM’s, however, require pharmacologic reversal prior to extubation to reduce
the risk of postoperative weakness. Once TOF monitoring reveals some return
of twitch response, anticholinesterase medication may be administered to raise
the endogenous levels of ACh at the neuromuscular junction. Acetylcholine
then floods the neuromuscular junction and overwhelms the residual non-
depolarizing NMB allowing for recovery of muscle strength. Neostigmine is
the drug of choice for reversal and typical dosing is 0.06mg/kg with a
maximum dose of 5 mg. Unfortunately, the rise in ACh caused by inhibition of
acetylcholinesterase is not isolated to the neuromuscular junction. The
systemic rise in plasma ACh can cause negative effects elsewhere by binding
muscarinic ACh receptors throughout the body resulting in adverse effects
such as bradycardia, bronchoconstriction and hyperperistalsis of the GI tract.
These effects are prevented by co-administration of an anticholinergic
medication such as glycopyrrolate which blocks the effect of ACh at the
34 Jeffrey Oldham
muscarinic ACh peripheral receptors while having no effect at the nicotine

ACh receptors found at the neuromuscular junction. Glycopyrrolate is
typically administered in doses of 0.2 mg for every 1mg of neostigmine given.
Discussion of reversal of neuromuscular blockade would not be complete
with mention of sugammadex. This newly approved medication binds
rocuronium and vecuronium rendering them inactive. No recovery of TOF is
required before administration of sugammadex and there are no adverse
cholinergic effects as seen with neostigmine. Sugammadex is administered as
a 2-4 mg/kg dose.
REFERENCES
[1] James R, Glen JB: Synthesis, biological evaluation, and preliminary
structure-activity considerations of a series of alkylphenols as
intravenous anesthetic agents. J. Med. Chem. 23: 1350-1357, 1980.
[2] Reves JG, Glass PS, Lubarsky DA, McEvoy MD, and Martinez-Ruiz R.
“Intravenous Anesthetics.” Miller’s Anesthesia. Ed. Ronald D. Miller.
7th ed. Philadelphia: Churchill Livingstone Elsevier, 2010. 719-768.
Print.
[3] Dundee J, Zacharias M: Etomidate. In: Dundee J (ed.): Current Topics in
Anesthesia Series 1. London, Arnold, 1979, p 46.
[4] Wagner RL, White PF. Etomidate inhibits adrenocortical function in
surgical patients. Anesthesiology. 1984 Dec;61(6):647-51. x. Pasternak
JJ, and Lanier WL. “Diseases Affecting the Brain.” Stoelting’s
Anesthesia and Coexisting Disease. Roberta L. Hines. Saunders, 2012.
218-254.
[5] White PF, and Eng WR. “Intravenous Anesthetics.” Clinical Anesthesia.
Ed. Paul G. Barash, Bruce F. Cullen, Robert K. Stoelting, Michael K.
Cahalan, and M. Christine Stock. 6th ed. Philadephia: Lippincot
Williams and Wilkins, 2009. 444-64. Print.
[6] Fukuda K. “Opioids.” Miller’s Anesthesia. Ed. Ronald D. Miller. 7th ed.
Philadelphia: Churchill Livingstone Elsevier, 2010. 769-824. Print.
[7] Coda BA. “Opioids.” Clinical Anesthesia. Ed. Paul G. Barash, Bruce F.
Cullen, Robert K. Stoelting, Michael K. Cahalan, and M. Christine
Stock. 6th ed. Philadephia: Lippincot Williams and Wilkins, 2009. 465-
497. Print.
[8] Egan TD. “Opioids.” Basics of Anesthesia. Ed. Ronald D. Miller and
Manuel C. Pardo. 6th ed. Philadelphia: Elsevier, 2011. 115-27. Print.
[9] Komatsu R, You J, Mascha EJ, Sessler DI, Kasuya Y, Turan A. A

nesthetic induction with etomidate, rather than propofol, is associated
with increased 30-day mortality and cardiovascular morbidity after
noncardiac surgery. Anesth. Analg. 2013;117:1329-37.
[10] Perouansky M, Pearce RA, and Hemmings HC. “Inhaled Anesthetics:
Mechanisms of Action.” Miller’s Anesthesia. Ed. Ronald D. Miller. 7th
ed. Philadephia: Churchill Livingstone Elsevier, 2010. 524. Print.
Chapter 4
PEDIATRIC ANESTHESIA
FOR THE NON-ANESTHESIOLOGIST
Raeford E. Brown, Jr., MD, FAAP

Anesthesiology and Pediatrics,
The safe perioperative care of infants and children requires the best efforts
of the child’s primary care providers as well as the physicians and nurses
whose job it is to provide safe care before, during, and after surgery. The
sophistication of anesthetic care has grown remarkably over the last quarter
century. This growth has allowed even children with significant medical
conditions to undergo surgery safely. Throughout the first half of the
twentieth-century, infants and children with congenital anomalies, pyloric
stenosis or heart disease were at high risk of mortality. Changes in the training
of a cadre of pediatric anesthesiologists, a better understanding of the
physiology attendant to the transition from the fetal state, safer anesthetic
medications, and the recognition of intrinsic risk factors are but a few of the
hundreds of changes in practice that have made for safe perioperative care for
children.
In this chapter, I hope to identify features of the care of children that are at
the interface between pediatrics and anesthesiology. By doing this, I hope to
communicate the important place that the primary pediatric care provider has
38 Raeford E. Brown, Jr.
in safe perioperative care. Also, I hope to reveal to the pediatric community

the thought processes that anesthesiologists have daily.
PERIOPERATIVE ASSESSMENT
OF THE CHILD
Pediatric Anesthesiologists think of themselves, on their best day, as the

pediatrician in the operating room; the explorer that finds hidden disease, the
protector of children brought into strange circumstances. In reality,
perioperative clinicians need to become masters of the focused assessment,
taking information already known and adding to it characteristics that will
affect the conduct of anesthesia and surgery. Of interest to an anesthesiologist:
1) The developmental level of the child – The operating room is a

frightening place for children, some more than others. From age 18
months to age five, most children harbor extreme anxiety about
leaving their parents, going with strangers, and entering a new
environment. Many children become inquisitive after age five and
require only explanations, toys, and an iPhone to separate from their
parents and go to the OR. Children with chronic disease, or who have
had one or more previous trips to the operating room cannot be fooled
and shouldn’t be. Most children respond to oral benzodiazepines by
becoming at ease. This change in behavior from fearful to happy is
good for parents and child. The best pediatric anesthesiologists, those
with many years of experience, pride themselves on their ability to
assess the level of anxiety of the child and the parents; a concerned
parent often begets an anxious child.
2) The presence of chronic disease – Most children are healthy but
many present for a surgical procedure with a history of a significant
systemic disease. Examples include the post premature infant with
chronic lung disease, the child with sickle cell anemia, or the patient
with cystic fibrosis. Anesthesiologists often have less information
about the patient's condition than is optimal. Parents may not know
the whole story or may be overwhelmed by the complexities of their
child disease. For these kids, the ability to communicate with the
primary care provider is critical to assuring safe anesthesia and
surgery. Good communication b be accomplished by giving the parent
Pediatric Anesthesia for the Non-Anesthesiologist 39
a business card so that when questions come up in the preoperative

assessment, the anesthesiologist can go to the source.
3) The presence of acute disease – Infants and children with a serious
illness that do not relate to the procedure at hand are critical to the
process of preoperative assessment. If a child is “sick,” has a fever,
feels bad, is vomiting, has diarrhea, and has a productive cough, they
should not come to the hospital or surgery center, much less the
operating room. A child that is ill will not feel better after any known
surgical procedure that is elective. A child that is sick will expose
other children and health care providers to their illness. Some will
expose their disease to patients that are immune compromised;
sometimes with a fatal outcome for that patient.
Some children have a runny nose every day. They are not sick per
se but have environmental allergies that produce sneezing, clear
rhinorrhea, and the “allergic salute.” For these children, the risk of
undergoing surgery and anesthesia is not elevated in the absence of
other more significant findings. Anesthesiologists are usually familiar
with these findings and are prepared to deal with an increase in airway
mucous. It is unnecessary to treat children with clear rhinorrhea and
no other clinical findings with antibiotics. The presence or absence of
these drugs will not change the thought process of the responsible
perioperative clinician.
4) The presence of an acute illness that requires urgent or
emergency surgery – Infants and children often present to the
operating room for surgical procedures e.g., necrotizing enterocolitis,
pyloric stenosis, abscess drainage. Many of these patients have
substantial metabolic disarray that must be managed emergently
before going to the operating room. In these circumstances pediatric
anesthesiologists and pediatric surgeons are well prepared to
resuscitate the child so that the surgical can be performed safely.
Many pediatric anesthesiologists and pediatric surgeons have
significant extra training in critical care; some pediatric
anesthesiologist are, in fact, board certified in pediatrics, having
chosen to have their pediatric practice in the perioperative arena.
When a child is ill, the need for high-quality rapid communication
between all caregivers is elevated substantially.
5) The presence of acute disease in a patient that has established
chronic disease - Children suffering from a severe disease associated
with chronic illness represent a unique group and require full
evaluation and management in the perioperative period. Infants that

are post premature with residual lung disease may develop Infectious
processes that can be deadly. Infection with the respiratory syncytial
virus (RSV) can produce refractory hypoxemia, sometimes requiring
hospitalization and ventilation. For this reason, children that are being
prepared for a surgical procedure by their primary care provider, are
post premature and have signs and symptoms suggesting lower airway
disease should not be considered appropriate for anesthesia or surgery
unless there is a risk for “life or limb,” a serious emergency.
Infants with residual heart disease, especially those partially
palliated for hypoplastic left heart disease, are similarly at risk for
mortality and morbidity when they develop even minor lower airway
disease. Patients with cystic fibrosis, sickle cell disease, or diabetes all
have elevated risk when an acute disease is superimposed. Again, it is
best practice to develop a plan for communication between primary
care provider and anesthesia care provider to reduce the risk for
chronically ill patients with acute disease.
PREOPERATIVE BEHAVIORAL STRESS IN CHILDREN

With upwards of three million children undergoing surgery in the United
States yearly, it has been estimated that about half suffer extreme preoperative
anxiety. This anxiety is characterized by feelings of nervousness, tension, and
fear. Some children manifest anxiety through well-developed physiologic
response such as tachycardia. A population of these kids has behavioral
responses including crying, hyperventilating, and increased motor tone. Some
will actively try to escape the medical professionals that are seeking to care for
them.
This response to the perioperative environment and the induction of
anesthesia has been identified as a terrifying aspect of the surgical experience.
Anxiety will often lead to difficulties in inducing anesthesia in the child and
may produce changes in behavior in the immediate post-operative period as
well as in the long term. Sleep and eating disturbances, new onset of enuresis
and encopresis and other novel behaviors may be identified in terrorized
children as long as two weeks after the operative event.
Several investigators have demonstrated that neuroendocrinological
changes occur in the setting of increased stress. Increased levels of cortisol,
endogenous catecholamines, growth hormone, and ACTH have been reported.
While the degree of change in observable physiologic parameters has been

evaluated, the degree of impact of variations in the neuroendocrine axis in the
whole organism is speculative at best. Thus, changes in wound healing and
immune function have been suggested but, thus far, not demonstrated. The
degree of behavioral response to painful stimuli in the anxious patient is,
however, an accepted clinical concept.
Because preoperative treatment of extreme stress in every child is uncalled
for – expensive and with its set of detractors – it is incumbent on the clinician
to recognize risk factors that will identify patients in which intervention is
required. Predictors that should be evaluated include age, parental anxiety,
temperament, social adaptability, coping style, and history of other medical
procedures.
Age
In general, children less than age one do not suffer separation anxiety and
children greater than six years old have developed coping skills sufficient to
carry them through induction of anesthesia.
These facts identify an age range – one year to six years - during which
there is a high probability of significant stress associated with leaving the
parents and going to the operating room. Children that have had multiple
medical procedures, especially those that have had adverse perioperative
experiences will often lag behind their peers in the development of coping
skills.
Parental Anxiety
It is a fact that children of anxious parents tend to be more anxious.

Whether that relates to inherited personality characteristics or subtle
communications between parent and child is not known. Similarly, the inborn
temperament of the child is often operative in producing greater or lesser stress
levels for any given situation.
Social Adaptability or Coping Style
Children deal with the stresses of life in a variety of different ways.

Avoidance mechanisms and catastrophizing are two mechanisms that do not
lend themselves to dealing well with everyday stressors. These children, when
identified, will usually have a better outcome if premedicated before leaving
the parent.
Children with Previous Medical Experience
Many children with chronic disease are forced to endure multiple surgical
procedures. This is relevant as long stays in the hospital tend to affect
psychosocial development in a detrimental fashion. A nine-year-old with
myelomeningocele who has undergone numerous shunt revisions and seems
entirely appropriate when first interviewed may ‘go to pieces' in the face of
another surgical procedure. The tendency among children with prior
experience to be intolerant of subsequent surgical procedures is magnified by
the lack of a stable care provider (e.g., parent or other).
How do we intervene to allay or reduce preoperative anxiety? The
methods of providing anxiolysis to children include behavioral and
pharmacologic intervention. Behavioral interventions include teaching coping
skills, modeling of appropriate behaviors, play therapy, operating room tours,
and providing printed material for parents to carry home. The practitioner’s
choice of which, if any, of these to include in the preoperative preparation will
depend on the resources available, the developmental level of the child and
whether the child has had previous surgical experience.
Parental presence in the operating room has been touted as an appropriate
method for reducing preoperative anxiety in children. The experimental
evidence, however, does not support this as a routine. In fact, in unselected
populations, parents in the operating room at the time of induction may
increase the level of anxiety for parent and child. Predictors of a successful
induction with the parent in the operating room include age greater than four
years, a calm baseline personality for the child and a gentle baseline
personality for the parent.
Pharmacologic Intervention
The use of anxiolytic compounds, such as benzodiazepines, for the

preoperative preparation of children has become accepted practice in the
United States. This practice has much to recommend it, but as with all drug
therapies, there are qualifiers.
Midazolam, now formulated with a cherry syrup compound produces
rapid anxiolysis and anterograde amnesia in children. Indeed for children in
the 18 months to 5-year time frame, this is overwhelmingly the method of
choice because the child readily accepts it as an oral formulation and the
mechanism of the benzodiazepines is familiar to parents. Respiratory
compromise with a dose of 0.75mg/kg is exceedingly rare. Occasionally this
dose will not provide sufficient sedation, and the practitioner should make a
decision about administering a second dose versus carrying the child
screaming to the OR.
Other premedicants, such as transmucosal (nasal) fentanyl and oral
ketamine are used occasionally, but preliminary studies with fentanyl
demonstrated side effects such as respiratory depression, nausea, and pruritus,
not usually seen with midazolam. Because of this side effect profile, the ease
of use of midazolam as well as the pharmacokinetic profile of the drug, it has
largely supplanted all other oral premedicants for children.
A positive outcome of surgical intervention for a child would include the
lack of the development of behavioral anomalies in the time after the surgery,
relative amnesia for the induction and a calm, compliant patient that can be
readily separated from the parent. Recent studies indicate that stress associated
with separation and the induction of anesthesia is, indeed, associated with the
development of postoperative adverse behavioral changes. These studies
suggest that parents be counseled about the possibility of the development of
enuresis, tantrums, nightmares and separation anxiety in children that
obviously have a less than ideal separation.
Physiologic outcomes associated with separation and the impact of these
findings on pain control, immunity, and wound healing are hard to quantify
now. It makes sense that changes in the neuroendocrine axis at the time of the
surgical procedure should adversely affect the child. These correlations are yet
to be demonstrated.
In summary, preoperative anxiety has a significant impact on children.
Those patients at highest risk can be identified. Methods are available for
pharmacologic and behavioral management of these patients.
PRE-EXISTING DISEASE THAT WILL DRAMATICALLY

AFFECT THE CONDUCT OF ANESTHESIA
There are some pathological processes that demand further analysis before
surgery. Some of these findings reflect genetic predispositions that are affected
by the anesthetics themselves. Some are problems that will require special
expertise beyond that of a general or community hospital, even when a
pediatric anesthesiologist is available. The primary care provider for the child
must have some understanding of these processes so that referrals are made to
the most appropriate medical center.
1) Cyanotic congenital heart disease – Infants that present at birth with

cyanotic congenital heart should be transferred to tertiary care
facilities with experience in managing this problem. Children with
residual disease postneonatal repair or palliative procedures with
complex hemodynamics require attention by practitioners familiar
with the child's surgical intervention and the risks involved in
anesthetizing the child. Interactions between the primary care
providers and the anesthesia care provider when children have
residual heart disease are especially important.
2) Metabolic anomalies producing acidosis – These aberrancies are
important during the perioperative period because they may interfere
with the metabolism of anesthetic drugs such as propofol. Often
systemic acidosis is identified through chronic growth failure.
Analysis of serum electrolytes before referral for surgery can assist in
making the diagnosis. Children that have not been stabilized through
diet or medication are at risk for hypoglycemia during periods of
starvation. For this reason, some children will require admission and
IV placement on the night before a surgical procedure so that a
reasonable NPO period can be accommodated.
3) Family history of malignant hyperthermia – If someone in a child's
family has a history of malignant hyperthermia, there is a reasonable
chance that they may also be affected. These kids should be cared for
by experts in the management of this disease. Despite wide
availability of a specific treatment, some children will die every year
because of failure to recognize and treat. (MH is reviewed in another
chapter in this book.)
4) Muscle disease - Patients with known dystrophies or infants with low

or no muscle tone often present to the operating room for muscle
biopsy. If the child has a dystrophy, volatile anesthetics will often
produce dramatic muscle breakdown and clearance of myoglobin in
the urine. If this happens, the child may develop acute renal failure.
Thus, these agents are to be avoided. For the floppy baby that comes
to the operating room for a muscle biopsy, the actual diagnosis cannot
be reasonably suggested from the clinical condition of the infant. In
this circumstance, volatile agents may be used but under close
supervision. Some practitioners will use total intravenous anesthesia
only with pain control via the use of local anesthetics.
Floppy babies are at high risk for ventilatory insufficiency after
general anesthesia and may develop frank apnea during the
postoperative period. For this reason, these infants should be
monitored in a high acuity unit for at least twelve hours or until the
baby's behavior has returned to baseline.
5) Infants with anatomic anomalies of the mandible or mid-face –
There are many congenital defects involving the midface. They are
important largely because of the respiratory embarrassment that
accrues from abnormal anatomy which may produce airway
obstruction in the anesthetized child. Hemifacial microsomia, Apert
syndrome, Pierre Robin syndrome and Crouzon syndrome are
important to the anesthesiologist because children that are reasonably
compensated under normal conditions may become impossible to
mask ventilate after the induction of general anesthesia. Most
anesthesiologists that manage children with midfacial anomalies want
all of the information that they can get as early in the planning of an
operative procedure as possible so that preparations for difficult
airway management can be made expeditiously.
6) Post premature infants with advanced residual pulmonary disease
– Some children born at less than 38 weeks post conceptual age will
develop lung disease with acute hypoxia during the first few days
after delivery. The inflammatory response associated with inadequate
surfactant, in conjunction with other common comorbidities such as a
patent ductus arteriosus, nutritional failure, or infection may take two
forms – acute and chronic. Severe disease can respond to noninvasive
ventilation, CPAP, and surfactant augmentation. Hypoxia that
continues for more than five to seven days may represent a change in
the configuration of the alveoli with increase collagen and fibrosis.
The residual disease may last for days or weeks and children that
require surgical intervention during that time are at risk of
exacerbation and should have expert care by practitioners familiar
with acute and chronic respiratory care in infants.
THE SAFETY OF GENERAL ANESTHETIC AGENTS

IN THE DEVELOPING BRAIN
General anesthetic agents, including volatile agents such as sevoflurane,

intravenous agents such as propofol, and sedatives such as midazolam have
been shown to produce cell death in the developing nervous system of nearly
all laboratory animals, including primates. Some amount of cell death is
normal in the developing brain, but it appears that anesthetics may accelerate
this process when given at high doses for extended periods of time. Studies
have also shown developmental delay in animals after exposure to anesthetics
for hours at a high dose. Many human studies from disparate populations do
not show developmental abnormalities of cognition and memory after short,
low dose anesthetics. Of course, no pathological specimens of human infants
and children after anesthetics are available and will certainly not be available.
It is an open question what the age sensitivities are, what the exact
mechanisms are, or if there is an effect on development in humans, what could
be done to reduce harm.
Clinicians and scientist from the FDA recently issued a warning about the
established evidence of toxicity in infants. This document reviewed that
information that is known and cautioned parents and physicians and nurses
that care for children to be cautious about the administration of general
anesthetics to children up to age three. Conversations about these issues should
be discussed with pediatric anesthesiologists, clinicians trained to provide for
the safety of infants and children during the perioperative period.
COMMUNICATION BETWEEN PRIMARY CARE PROVIDERS

AND ANESTHESIA CARE PROVIDERS
Although policies vary widely, communication between the child’s

primary care provider and the anesthesia care provider is in the child’s best
interest and should be considered best practice. The primary care provider
knows the family, the child and any interactions that may play a role in safe
perioperative management. There is often anxiety about the interactions
between anesthesiologists and primary care providers; there should not be.
Both teams want the best for the children that they care for and only by
developing plans for maintaining professional relationships will these patients
receive the care that they need.
CONCLUSION
Management of infants and children during the perioperative period often
requires knowledge of superimposed acute and chronic disease processes,
genetic abnormalities, metabolic disturbances, as well as an understanding and
sensitivity to the social milieu that the child inhabits. Critical to providing the
best care for any child is a caring clinician that is capable of interacting with
others to define all problems and produce rational solutions. Communication is
essential, and the sicker, younger, or more involved the patient's care is, the
more important is the relationship between all care providers.
Chapter 5
OBSTETRIC ANESTHESIA FOR

THE NON-ANESTHESIOLOGIST
Lori C. Kral Barton, MD

In any discussion of obstetric anesthesia, attention must be paid to the

physiologic changes of pregnancy and their anesthetic implications. Starting in
the first trimester, hormonal changes work to meet the demands of the growing
fetus and placenta. The evolving physiologic environment of the parturient
must be considered when evaluating her for an anesthetic.
CENTRAL NERVOUS SYSTEM

During the first trimester of pregnancy and throughout the postpartum
period, the minimal alveolar concentration (MAC) is decreased by as much as
30% and remains decreased throughout the pregnancy. Pre-pregnancy
anesthetic requirements return by 72 hours postpartum [1-3]. Progesterone
(a central nervous system depressant) and increased plasma endorphins are
thought to be primarily responsible for this decrease in MAC [1]. The
increased amount of circulating progesterone initially comes from the corpus
50 Lori C. Kral Barton
luteum. By week 10 of the pregnancy, the placenta takes over the role of
producing progesterone.
The time of anesthetic induction is also decreased due to increased minute
ventilation combined with a decreased functional residual capacity (FRC). In
pregnant females, alveolar concentrations of inhalational anesthetic approach
inhaled concentrations of anesthetic more quickly than their non-pregnant
cohorts. This decreased time to induction occurs despite increased cardiac
output, which would normally prolong inhalational induction rather than
hasten it.
The amount of local anesthetic needed in pregnancy is also decreased due
to increased sensitivity as well as decreased cerebral spinal fluid (CSF) when
intrathecal techniques are used [4]. Decreased local anesthetic requirements
are seen as early as the first trimester, making some of the anatomic changes
that are seen in a more advanced pregnancy only partially to blame. It is not
completely understood when the reduced dose requirements return to pre-
pregnancy levels; however it has been shown that patients undergoing
postpartum tubal ligation have increased spinal dose requirements as
compared to women undergoing cesarean section [5].
CIRCULATORY AND HEMATOLOGIC SYSTEMS

Beginning in the first trimester of pregnancy until approximately two
weeks postpartum, hemodynamic changes driven by hormones cause
numerous cardiovascular changes in the parturient.
Prior to placentation, the corpus luteum produces relaxin, a peptide
hormone that demonstrates vasodilatory effects. Levels of relaxin continue to
rise throughout the early stages of the pregnancy and peak at the end of the
first trimester [6]. Similarly, increased levels of prostacyclin (PGI2), and
progesterone throughout the pregnancy contribute to further decreases in blood
pressure due to relaxation of smooth muscle [7]. Systolic blood pressure,
diastolic blood pressure, and mean arterial pressure continue to decrease until
reaching the nadir in the second trimester. The blood pressure then continues
to rise slowly until values close to pre-pregnancy are reached near term [6].
Changes in cardiac output increase significantly in the first trimester
primarily due to increases in heart rate which will rise by 10-20 beats per
minute from baseline to term [8]. Later in the pregnancy, the increased cardiac
output is increased primarily by stroke volume which is driven by increases of
estrogen [9].
Obstetric Anesthesia for the Non-Anesthesiologist 51
Increased plasma volume from as early as 6 weeks gestation affects the

cardiovascular system as the pregnancy progresses [10]. Rising levels of
estrogen cause increased activity of the renin angiotensin aldosterone system
(RAAS). The effects of this RAAS activation cause plasma volume to expand
about 45% above baseline [10, 11]. Concurrently, there is also a rise in
erythropoiesis about 40% above baseline. These discordant increases account
for the dilutional anemia of pregnancy causing the mother’s hematocrit to
reach a new average value of 34% by the third trimester. This level does not
return to pre-pregnancy values until 6 weeks post-partum [12].
Increases in both preload and afterload lead to an increase in volume of all
four heart chambers, and increased left ventricular wall thickness. These
temporary changes contribute to atrial dysrhythmias and flow murmurs heard
during pregnancy.
As plasma volume increases, most of the coagulation factors (Factors I,
VII, VIII, IX, X, XII) also increase making pregnancy a hypercoagulable state
that can be seen in a thromboelastogram (TEG). These changes remain until
the second week postpartum when the coagulation factors return to the non-
pregnant state. This hypercoagulable period increases the risk of
thromboembolism during pregnancy and the postpartum period six-fold [13].
Second to anemia, thrombocytopenia is the one of the most common
hematologic abnormalities encountered during pregnancy. Approximately 5%-
10% of parturients have platelet counts less than 150 x 109 /L. Of those cases,
70-80% are related to gestational thrombocytopenia. It is speculated that
increased platelet clearance as well as dilutional thrombocytopenia are the
primary causes [14-15]. As long as platelet values remain above 70 x 109 /L,
and no other etiology is suspected (Preeclampsia/HELLP) no further
investigation is warranted. If platelet quantity and quality are of concern,
either a thromboelastogram (TEG) or a platelet function assay 100 (PFA 100)
can be done to understand the functionality of the platelets. Thrombocytopenia
of pregnancy usually resolves by 6 weeks postpartum and can return with
subsequent pregnancies.
As the fetus continues to grow beyond 20 weeks gestation, avoiding the
supine position in the parturient has to be of paramount concern. After 20
weeks of gestation, compression of the inferior vena cava and the aorta,
collectively known as aortocaval compression, can cause decreased uterine
blood flow and preload to the maternal heart. As the pregnant woman gets
closer to term, lying on her left side helps to alleviate the compression. During
procedures when the parturient is expected to lie supine (cesarean
section/cerclage), having the bed tilted laterally at an angle of 30° increases

the amount of inferior vena cava return [16].
Respiratory System
Numerous mechanical changes to the thoracic cavity help account for the
multiple respiratory changes that accompany pregnancy. The increased oxygen
requirements during pregnancy combined with the increased uterine size drive
many of the changes to the respiratory system during pregnancy. Early in
pregnancy, relaxin release increases thoracic cage mobility allowing for the
subcostal angle to increase. The lower rib cage circumference also increases
by about 5 cm. allowing for increased tidal volumes [17]. In addition, the
diaphragm also rises leading to a decrease in FRC.
FRC can be thought of as the remaining oxygen in the lungs after a patient
exhales such as during periods of apnea. Combining the increased oxygen
consumption of the fetus and the placenta with the decreased FRC, it is
understandable why a parturient desaturates faster than a non-pregnant female.
This reduced apnea tolerance becomes important during times of general
anesthesia or during eclamptic seizures.
Minute ventilation increases during pregnancy primarily due to increased
tidal volumes rather than a significant increase in respiratory rate. Because of
the increased progesterone in the first trimester, minute ventilation increases
leading to a respiratory alkalosis despite an increase in the amount of carbon
dioxide production. As a result new baseline blood gas values are seen,
allowing for a mildly decreased PaCO2, PaO2, increased pH, and decreased
bicarbonate.
Upper airway changes have the potential to complicate airway
management in the pregnant woman. Capillary engorgement of the respiratory
mucosa makes the tissues very friable. Increased progesterone levels cause
further edema of the upper airways potentially making intubation and airway
management difficult.
Gastrointestinal System
In the past it was thought that decreased gastric emptying occurred during
pregnancy. But numerous studies have shown gastric emptying does not slow
during pregnancy [18]. However during active labor gastric emptying does
slow regardless of opioid administration, and is exacerbated by the use of

opioids in labor analgesia.
Numerous mechanical changes to the parturient anatomy increase the
pregnant woman’s risk for aspiration. As the gravid uterus continues to grow,
the stomach, liver and intestines demonstrate a cephalic displacement. The
gastroesophageal junction also becomes displaced allowing for portions of the
lower esophagus to move into the thoracic cavity. Progesterone also decreases
the tone of the lower esophageal sphincter potentially allowing gastric contents
to reflux into the esophagus. Progesterone does not cause the same sphincter
relaxation of the upper esophageal sphincter (UES) since the UES is primarily
striated muscle rather than smooth muscle [19, 20]. As many as 50% of
pregnant women experience gastroesophageal reflux during their pregnancies
and that risk increases with a history of reflux prior to pregnancy.
Further changes in the gastrointestinal system include increased biliary
stasis also as a result of the increased progesterone, which slows gallbladder
motility. In fact, cholecystectomy is the second most common non-obstetric
surgery after appendectomy in pregnant women. With the increased risks
outlined above for aspiration, it is important when planning for a general
anesthetic to consider all parturients to have a “full stomach” despite their
NPO status.
Renal System
Increased plasma volume and vasodilation contribute to an increased

glomerular filter rate (GFR) and renal plasma flow. These increases allow for
a decreased serum urea, creatinine, and uric acid. As the pregnancy progresses,
kidney size increases as a result of dilated conducting systems allowing for a
30% increase in the volume of the kidney [21]. Increased stasis and volume
contribute to an increase in pyelonephritis that is seen in pregnancy.
Renal Tubular function is also altered as the amount of protein and
albumin excreted increases especially after 20 weeks gestation. During
pregnancy most women do not exceed 200mg/24 hours of proteinuria and
concerns of preeclampsia arise if the levels exceed 300mg/24 hours. Some
have speculated that the rise in proteinuria is as a result of the increase in
GFR: however the timing of the proteinuria does not correlate to the increase
in filtration rate [22].
Glucose is normally filtered from the glomerulus with reabsorption
occurring at the proximal tubule and to a small extent the collecting duct.
During pregnancy, there is less effective reabsorption combined with

variability in glucose secretion. Glucose absorption returns to pre-pregnancy
values approximately a week postpartum [21].
The respiratory alkalosis seen during pregnancy as a result of increased
minute ventilation is partially compensated for by the kidneys. Sodium
bicarbonate excretion increases to re-establish a baseline bicarbonate value of
20-21 mEq/L as compared to the non-pregnant value of 24 [23]. When
evaluating a blood gas of a parturient, these altered acid base values have to be
considered.
ANESTHESIA FOR THE LABORING PARTURIENT

Whether a woman undergoes a spontaneous or induced labor, the
progression of labor challenges the anesthesia provider with an evolving
picture of pain if the woman desires labor analgesia.
Classically, labor has been divided into three stages, with the first stage of
labor beginning when there are regular uterine contractions until complete
cervical dilation, generally considered 10cm for full term pregnancies. The
second stage of labor is the delivery of the baby. The final stage begins after
the delivery of the baby and is complete after placental delivery.
During the first stage, the pain that is experienced is visceral as the lower
uterine segment and cervix stretch to accommodate the descent of the fetus.
Afferent C fibers from the lower uterine segment and the cervix travel to the
dorsal root ganglia in the thoracolumbar region and the pain that is perceived
is referred to the dermatomes that are supplied by the same spinal cord
segments which receive input from the uterus and cervix [24]. During this first
stage of labor, getting coverage from T10-L1 dermatomes via a neuraxial
technique is considered the gold standard for labor analgesia offering the most
effective and least depressant analgesia.
As labor progresses the parturient enters stage two: when the cervix is
completely dilated until the birth of the neonate. The initial visceral pain from
stage one is now accompanied by somatic pain from the descent of the fetus
from the uterus to the vaginal vault. Afferent fibers from the vagina and
perineum join the pudendal nerve to converge at the dorsal root ganglia of S2-
S4. Re-dosing the epidural with more local anesthetic to cover the lower
dermatomes of S2-S4, or by pudendal nerve block, the somatic pain of labor
can be ameliorated.
The effects of labor pain on maternal and fetal physiology have been well
studied. The increase in maternal plasma catecholamines and the increased
respiratory effort with subsequent periods of apnea and consequent hypoxemia
can potentially lead to fetal hypoxemia. Increased epinephrine and
norepinephrine lead to increased maternal peripheral vascular resistance
followed by decreased uterine blood flow, which could potentially threaten a
fetus with insignificant reserves.
The American Congress of Obstetricians and Gynecologists (ACOG) have
changed their opinions on the timing of neuraxial analgesia. In the past,
recommendations regarding neuraxial analgesia timing encouraged delaying
epidural analgesia in nulliparous women until the cervix was dilated 4-5cm. At
that time research indicated that there was possibly a connection between early
epidural placement and the need for cesarean section. Later evaluation of the
research changed the recommendations of the ACOG. In a joint statement with
the American Society of Anesthesiologists in 2004, ACOG changed their
opinions:
“Labor causes severe pain for many women. There is no other

circumstance where it is considered acceptable for an individual to
experience untreated severe pain, amenable to safe intervention, while
under a physician’s care. In the absence of a medical contraindication,
maternal request is a sufficient medical indication for pain relief during
labor.” [25]
In a recent study including 1,829,302 singleton vaginal births to women in

27 states (this representing 65% of all U.S. singleton vaginal births in 2008)
61% received neuraxial anesthesia [26]. This majority of laboring parturients
is understandable given the safety and efficacy of neuraxial analgesia. Prior to
initiation of neuraxial anesthesia it is imperative to consider the absolute and
relative contraindications to placing a neuraxial anesthetic.
Absolute contraindications begin with patient refusal. Although patients
may change their mind about neuraxial anesthesia after their questions are
addressed or their misinformation is corrected, some patients will continue to
refuse even if it is in the best interest of them or their fetus. An example of this
is when there exists a high probability of cesarean section. During these cases,
it is important to educate the patient about the increased risks to both her and
the fetus if general anesthesia has to be used during an emergency. Ultimately,
regardless of the consequences, it is the patient’s right of autonomy that
determines the labor and analgesia management.
Further contraindications to neuraxial anesthesia also include:

uncooperative patient, thrombocytopenia, coagulopathy, infection at the site of
the neuraxial placement, uncontrolled hemorrhage or significant uncorrected
hypovolemia, allergy to local anesthetics, increased intracranial pressure,
unstable spine or spinal abnormalities either congenital or following previous
surgeries, unavailability of anesthesia providers trained in the technique. If
coagulopathy is a result of medications that the patient is taking, the American
Society of Regional Anesthesia and Pain Management (ASRA) has issued a
consensus statement addressing time to placement of neuraxial anesthetic,
catheter removal following anticoagulation, and time for re-dosing
anticoagulants when a neuraxial catheter is indwelling. If a patient is on any
anticoagulant medications it is imperative to refer to their guidelines before
proceeding with the anesthetic.
When considering thrombocytopenia, there is not a definitive cutoff value
when deciding if neuraxial placement is appropriate. Multiple variables have
to be considered including the cause of the thrombocytopenia, the recent trend
of the patient’s platelets, the quality of the patient’s platelets, other causes
contributing to a coagulopathy, the quality of the patient’s airway, as well as
other co-morbidities. Considering there is a lack of data to suggest that a
specific platelet count predicts the risk of spinal epidural hematoma in the
obstetric population, each patient and the confounding variables that cloud the
picture have to be considered.
Thrombocytopenia is defined as platelet counts less than 100,000/mm3
although in a study from 1996, of the 306 anesthesiologists in the United
States that were polled, 60% indicated that they would place an epidural if
platelet counts were between 80,000-100,000/mm3 in healthy parturients [27].
Of note, the risk of spinal epidural hematoma in the obstetric population is
lower compared to elderly patients receiving neuraxial anesthesia for
orthopedic procedures. As in all medical decisions, the benefit of the
procedure must outweigh the risks of the intervention and each patient must be
individually assessed.
Three principal neuraxial techniques can be considered for the
management of labor pain; epidural, combined spinal-epidural (CSE) or
continuous spinal with an intrathecal catheter. Although a single shot spinal
can be considered, often the duration of labor outlasts the single dose of
anesthetic making it an impractical option. The choice of neuraxial technique
is dictated not only by patient preference but also maternal comorbidities,
obstetric concerns, and anesthetic considerations and preferences.
Epidural anesthesia with catheter placement is the most common of the

three options. One of the biggest advantages of epidural analgesia includes
maintenance of analgesia as long as the epidural catheter remains in place.
Analgesia is maintained by either repeated bolus dosing or via a continuous
infusion with available bolus dosing if needed. A second significant benefit of
epidural anesthesia is the ability of using the epidural catheter for epidural
anesthesia in cases that have to be converted to cesarean section thus avoiding
general anesthesia. In patients who have pre-load dependent pathology or who
are intolerant of a decreased peripheral vascular resistance, epidural analgesia
offers the option of slow dosing thus minimizing the neurocardiogenic effects
that occur when a sympathectomy follows.
Nerve fibers that affect vasomotor tone of the arterial and venous vessels
come from T5-L1 and the sympathectomy that follows neuraxial analgesia
blocks the sympathetic outflow leading to a venous and arterial vasodilation. It
is important to remember that the level of sympathetic blockade is higher than
the sensory level. Furthermore, uteroplacental perfusion can be compromised
with a decreased blood pressure since uterine blood flow is affected by
decreased perfusion pressure.
Uterine Blood Flow = Uterine Perfusion Pressure/Uterine

Vascular Resistance
Prehydration with crystalloid in healthy parturients without significant co-

morbidities can be considered around the time of the neuraxial placement to
counter the effects of the relative hypovolemia due to the sympathectomy.
Although most providers do administer some volume of crystalloid bolus, the
ASA Task Force on Obstetric Anesthesia has included in their practice
parameters that a fixed volume of IV fluid is not needed although it can be
used to reduce the frequency of maternal hypotension. The practice parameters
address volume pre-loading prior to spinal anesthesia and prior to cesarean
section yet no mention is made prior to epidural for vaginal delivery [28].
When epidurals are dosed with dilute solutions of local anesthetic, severe
hypotension is less likely.
Epidural catheters are ideally placed for the laboring parturient in the L2-
L3 or L3-L4 interspace. Epidural placement is a sterile technique. After the
epidural needle is seated into the interspinous ligament, a loss of resistance
after going through the ligamentum flavum is used to identify the epidural
space. Either air or saline is used in the syringe and no clear advantage exits of
one technique over the other. The catheter is threaded through the needle4-5
cm into the epidural space
Epidural test dosing is done prior to using the epidural for labor analgesia.
Although test dosing does not guarantee the location of the catheter, it helps
reduce the possibility of not recognizing either an intrathecal catheter or an
intravascular catheter. Small concentrated doses of local anesthetic and
epinephrine are injected while the patient is not under added discomfort of
contractions. A heart rate increase of 25-30 bpm over baseline would be
indicative of an intravascular catheter. If the patient were to develop a motor
block within five minutes of injection, the catheter would be considered
intrathecal and would be replaced. Another added safety measure that should
be added to routine epidural dosing is aspiration prior to injection. If CSF or
blood can be aspirated, the catheter should be replaced. Finally, portioning
each bolus dose into 5ml volumes will alert the anesthesia provider early
rather than late if catheter migration has resulted in either intrathecal or
intravascular placement.
Combined spinal-epidural (CSE) techniques are less common for labor
analgesia as compared to epidural catheters, but this technique offers some
advantages in certain patient populations. When placing the CSE, the initial
intrathecal dose of opioid and/or local allows for a quicker relief of labor pain
and better sacral nerve coverage, yet after the spinal medications of the CSE
have worn off, the epidural catheter can then be dosed for longer relief of labor
pain. Initiating analgesia with a CSE allows for decreased dosages of both
local or lipid soluble opioid decreasing the risk of fetal and maternal systemic
exposure.
A significant risk of CSE is the inability to verify that the epidural that
was placed at the time of the procedure is functioning properly. Although
epidural catheters as part of a CSE are more likely to be functional, this fact
cannot immediately be confirmed while the patient is able to get pain relief
from the spinal component of the CSE.
Continuous spinal analgesia is rarely employed as the initial plan for labor
analgesia. After an unintentional dural puncture during epidural placement, a
catheter might be thread into the intrathecal space rather than reattempting
epidural placement. If the anesthesia provider chooses to maintain the
intrathecal catheter, communication with the nursing staff, and obstetrics team
has to be clear that the catheter is intrathecal to prevent overdosing since
intrathecal dosages are significantly less than epidural dosages. Clear labeling
of the catheter as intrathecal and possibly a sign over the patient’s bed should
indicate the catheter position.
In some patient populations, planning for an intrathecal catheter as the

initial strategy for analgesia might be a very appropriate choice despite the risk
of post dural puncture headache. In patients who have a strong risk for surgical
delivery and have a difficult airway whose neuraxial placement was difficult,
as might be seen in a morbidly obese patient, having continuous verification of
a functioning neuraxial catheter is imperative. The risk of post dural puncture
headache may be decreased in the morbidly obese parturient as compared to
patient’s with a decreased body mass index (BMI). Multiple studies have
addressed this with conflicting results [29, 30, 31].
Although neuraxial analgesia provides the most effective and least
maternal depressant analgesia for comfort, IV analgesia and inhaled
anesthetics can be used. If neuraxial analgesia is contraindicated, the parturient
refuses, or if regional analgesia is unavailable, systemic analgesia can provide
some relief.
The most common inhalational anesthetic in obstetrical anesthesia is
nitrous oxide (N2O). This form of analgesia is commonly used in the United
Kingdom with 60-75% of parturients using it compared to the United States,
where its limited availability and maternal preference for neuraxial analgesia
limits nitrous oxide use to about 1% [32]. Although the long-term effects on
the fetus are unknown, studies have indicated that nitrous oxide could
potentially have neurotoxic effects on the fetal brain; however its effects are
not fully understood. Unlike parenteral opioids used for labor analgesia,
maternal nitrous oxide use does not affect Apgar score or umbilical artery or
vein blood gases [32, 33]. This is despite the mild respiratory depressant
effects of nitrous oxide. If opioids are used in combination with nitrous oxide,
further respiratory depression develops and is evident in decreased maternal
oxygen saturations. Maternal satisfaction with the use of nitrous oxide varies
with multiple studies showing that although visual analog pain scores had
minimal if any decrease when compared with air, most women would choose
to use nitrous oxide for subsequent labors [32].
Although studies have indicated superior maternal pain relief during labor
with sevoflurane as compared to nitrous oxide, increased risk of maternal
sedation, loss of protective airway reflexes, lack of delivery equipment and
superior neuraxial techniques make inhalational sevoflurane an unpopular
analgesic option currently in the United States [34].
Parenteral analgesia with systemic opioids remains the most common
form of labor analgesia worldwide. Ease of administration, low cost, and
availability boost their popularity and when contraindications for neuraxial
analgesia exist, they offer another option for pain management for the
anesthesia provider. Disadvantages of parenteral opioids include less effective

analgesia as compared to regional analgesia, increased nausea and vomiting,
maternal and fetal sedation as evidenced by decreased fetal heart rate
variability and maternal hypoventilation, and decreased gastric motility. Due
to the low molecular weight and lipid solubility of opioids, all opioids can
cross the placenta with IV administration leading to increased fetal systemic
levels as compared to opioids given via the neuraxial route due to the greater
dosing requirements.
Delivery of IV opioids can be done with either intermittent bolus dosing
or patient controlled analgesia pumps (PCA). PCA delivery with opioids can
be offered with or without a continuous background infusion. Maternal
satisfaction using PCA with opioids is increased as compared to bolus dosing
possibly due to the ability to achieve a more stable drug concentration despite
not being able to demonstrate a decrease in total narcotic delivery. Limited
worldwide availability of equipment prevents PCA delivery of systemic
opioids from surpassing intermittent bolus dosing in popularity.
Worldwide, meperidine is the most common opioid employed during
labor owing to its ease of use, availability and low cost. The perceived effects
of meperidine have probably as much to do with maternal sedation as
compared to its analgesia effect owing to significant effects on the fetus [35,
36]. The onset of effect is 5-10 minutes after IV administration and the
duration is between 2-3 hours. Metabolism is by the liver into normeperidine,
an active metabolite that can continue to cause respiratory depression. Bolus
dosing is preferred to PCA dosing for meperidine due to increased
accumulation of the drug and its metabolite causing concern for continued
maternal respiratory depression and decreased fetal Apgar scores. The time to
peak fetal uptake is 2-3 hours after maternal dosing and neonates born during
this interval have been shown to be susceptible to respiratory depression.
Maternal satisfaction with analgesia after meperidine varies, with most
indicating improved pain scores as compared to placebo, yet overall
satisfaction was limited [37, 38].
Like meperidine, morphine metabolism includes an active metabolite that
also causes respiratory depression. In addition to respiratory depression,
morphine-6-glucuronide also delivers continued analgesia offering a duration
time of 3-4 hours. These characteristics make morphine less ideal for a PCA
delivery system increasing concern for neonatal depression. With a longer
length of duration, morphine might appear like an attractive option for pain
control early in labor however multiple studies conclude that poor maternal
pain control combined with increased maternal sedation make IV morphine a
less viable option [39, 40, 41]. Although all opioids cross the placenta, the
quick transfer of morphine across the placenta makes it less ideal as an
analgesic. This combined with delayed fetal clearance and maternal sedation
makes the safety profile of morphine less attractive in the labor suite.
Mixed agonist-antagonist opioids like butorphanol and nalbuphine offer a
ceiling effect for respiratory depression, which is more attractive when larger
doses are given for pain control. Both drugs have high maternal placental
transfer, yet still lower than morphine comparatively. Although both opioids
lead to maternal sedation and fetal transfer of drug, there is little evidence to
support long term significant fetal or neonate depression. When considering
the effectiveness of both drugs for maternal pain relief, multiple studies have
shown similar pain scores with adequate pain relief when compared to
meperidine [42, 43]. Duration of analgesia varies between the two drugs with
butorphanol lasting 3-4 hours and nalbuphine lasting 3-6 hours.
Fentanyl, a synthetic opioid remains a popular option for labor analgesia
since the placental transfer is significantly less as compared to the opioids that
have previously been discussed. Capable of being used as a bolus dose or via
patient controlled analgesia pump, the flexibility of fentanyl also makes it an
attractive option and unlike meperidine and morphine, fentanyl lacks active
metabolites. Several studies have found that systemic fentanyl is more
effective in managing labor pain when compared to meperidine [44, 45]. Like
most opioids, systemic fentanyl causes decreased fetal variability however no
significant differences in Apgar scores or neonatal neurobehavioral side
effects were found [44]. When fentanyl was used in PCA dosing regimens for
up to five hours it was well tolerated. Of the infants in this study, 37%
required naloxone at some time while their oxygen saturations were measured
over a 12 hour period [46].
Remifentanil is a unique opioid due to its pharmacokinetics and
pharmacodynamics making it a more ideal drug for PCA dosing as compared
to other opioids. Remifentanil has a rapid onset of action (about 1 minute) and
is broken down by plasma esterases to inactive metabolites, which are
eliminated by the kidneys. Although there is rapid transfer across the placenta
into fetal circulation there is also rapid breakdown by the fetus thus limiting
the depressant effects on the fetus. Like fentanyl, the efficacy of remifentanil
has been validated when compared with IM meperidine. Although remifentanil
appears in many ways like an ideal alternative to neuraxial analgesia it cannot
be over looked that it can cause significant respiratory depression [47].
Because of this, when considering remifentanil for labor analgesia, it is
recommended that continuous pulse oximetry and one on one nursing be used.
ANESTHESIA FOR CESAREAN DELIVERY

Numerous reasons contribute to the fact that cesarean delivery is one of
the most common surgical procedures performed in the United States.
Maternal choice, cephalopelvic disproportion, previous uterine surgery,
placental abruption, placenta previa, infection, fetal intolerance to labor, and
umbilical cord prolapse, are a few of the reasons for the choice of cesarean
delivery over vaginal birth. Although cesarean section is the best choice in
some cases for both the mother and the fetus, it is important to realize that
cesarean section can further complicate subsequent pregnancies. The risk of
placental abruption, placenta previa, and uterine rupture following attempt at
vaginal delivery after cesarean section are all increased. Increased recovery
time, increased risk of infection, post-operative ileus, and increased risk of
thrombosis are immediate potential complications that also have to be
considered.
As with any patient interaction, the anesthesia provider constructs the
anesthetic plan carefully after a focused history and physical. The practice
guidelines direct the initial evaluation to include maternal health and
anesthetic history, a focused obstetric history, baseline blood pressure
measurements, and an exam of the heart, lungs, and airway. The nature of the
cesarean section, if emergent or elective, also contributes to the choice given
that general anesthesia allows for the shortest time to skin incision once an
emergency is identified. If a parturient is a candidate for neuraxial anesthesia,
and time permits placement of a neuraxial block, then this should be the
preferred method due to increased risks to both maternal and fetal well-being
under general anesthesia.
Maternal mortality during cesarean section is increased in general
anesthesia as compared neuraxial anesthesia with failed intubation and
maternal aspiration leading the list of complications. It is estimated that 1 in 30
obstetric intubations will be difficult, as compared to 1.8% in the general
population [48, 49]. General anesthesia in cases of difficult intubation can be
catastrophic to both mother and fetus resulting in morbidity and mortality for
both patients.
Contributing to the increased rate of difficult intubation is increased
airway edema due to increased maternal estrogen. Not only does the airway
evaluation change throughout the pregnancy, but also acute changes can be
seen as the parturient advances through labor [50]. Further obstacles to easy
intubation include increased friability of airway tissues potentially leading to
poor visualization, pre-eclampsia with increased airway edema, increased
body mass index from weight gain during pregnancy, and enlarged tongues
making direct visualization challenging.
In cases where difficult intubation is anticipated, it is imperative to have
multiple trained personnel as well as difficult intubation equipment available.
In these cases, establishing early neuraxial analgesia with a working epidural
is ideal if there are no contraindications. Another consideration in cases of
known difficult airways is establishment of an indwelling intrathecal catheter
allowing for continuous spinal analgesia during labor. In these cases, if the
patient had to proceed to the OR emergently for a cesarean section, aspiration
of CSF through the catheter would establish conformation of a working spinal
catheter thus bypassing the need for general anesthesia in a known difficult
intubation patient. The risk of a postdural puncture headache for the benefit of
avoiding general anesthesia is a tradeoff most anesthesia providers would
accept. In cases where neuraxial anesthesia is not an option and the patient is
an anticipated difficult intubation, awake intubation is the safest option.
Maternal aspiration under general anesthesia also contributes to maternal
morbidity and mortality. As discussed previously, pregnancy increases the risk
for aspiration due to the numerous physiologic changes to the gastrointestinal
system. In 1946 Dr. Curtis L. Mendelson, an obstetrician, wrote an article
describing the aspiration of stomach contents into the lungs leading to a
chemical pneumonitis. He postulated that as little as 25 ml. of gastric acid can
lead to the development of a chemical pneumonitis with tachypnea and
hypoxia developing within 2-5 hours after the aspiration event. The clinical
picture can evolve into acute lung injury or acute respiratory distress syndrome
(ARDS) requiring mechanical ventilation or ICU management.
During emergency cesarean section, all precautions should be taken prior
to induction of general anesthesia to decrease the likelihood of aspiration
including cricoid pressure and 30 ml of a non-particulate antacid such as
sodium citrate, which increases the gastric pH. Care should also be taken at the
end of the anesthetic since extubation is also a period of increased risk of
aspiration. Prior to emergence of general anesthesia, suctioning of stomach
contents via an oral gastric tube can decrease the amount of gastric volume
and further decrease the risk.
Initiation of the anesthetic induction should begin only after the patient
has had adequate pre-oxygenation with 100% oxygen via facemask, her
abdomen has been prepped and draped, and the obstetric team is bedside at the
operating room table ready for incision. Decreasing the amount of time that
the fetus is exposed to the induction agents decreases the likelihood of
neonatal depression. Maintaining left uterine displacement is also required to
decrease the risk of utero-placental malperfusion. A rapid sequence induction

with an IV induction agent followed by an IV dose of succinylcholine can be
administered quickly with little effect on the fetus. After conformation of
correct tube placement, the obstetric team can proceed.
Maintenance of anesthesia is achieved with volatile agent in combination
with nitrous oxide. After the delivery of the fetus and uterine tone is needed,
the volatile agent is decreased and nitrous oxide and opioids can be used to
supplement the anesthetic. High dose volatile anesthetic agents can cause
uterine relaxation and this increased atony can easily lead to maternal
hemorrhage [52]. Oxytocin, the first line agent for uterine atony is also given,
however it is given diluted into a 500ml to 1 liter of crystalloid due the risk of
hypotension with an IV bolus.
The gold standard anesthetic for cesarean section remains neuraxial
anesthesia when there are no contraindications. The choice between a single
shot spinal anesthetic versus an epidural, versus a combined spinal epidural
(CSE) requires the consideration of numerous variables. If the patient has an
indwelling epidural catheter from labor analgesia, increasing the anesthetic
coverage by achieving a higher, denser block (most commonly with lidocaine)
is the best option. If the cesarean section is urgent yet not emergent and time
permits placement of a combined spinal epidural, you get the benefit of rapid
analgesia from the spinal yet the options for continued analgesia when the
spinal has worn off. In patients with anticipated difficult airways, CSE
anesthesia is avoided since the epidural that was placed has not proven to be
functional and urgent general anesthesia would have to be implemented if the
spinal anesthesia wore off and the epidural failed. In numerous centers, single
shot spinal anesthesia is routinely used when cases are predictably short and
terminate within the time restraints of the spinal.
When indwelling epidural catheters are in place from a laboring parturient,
lidocaine 1.5%-2% offers the benefit of intermediate onset of action and a
reasonable duration of action. When bicarbonate is added to the lidocaine
dosing it hastens the speed of onset. The addition of epinephrine to lidocaine
increases the maximum dose of lidocaine that the patient can get and thus
decreasing the chance of local anesthetic systemic toxicity (LAST). When
epinephrine is added to the lidocaine, not only does it increase the dosing
available, but the duration of action is increased thus prolonging the epidural.
Extending the block so that it reaches a cephalad spread between T2-T6 will
allow adequate pain control even if exteriorizing of the uterus by the
obstetricians is needed to achieve good hemostasis.
When a functional indwelling epidural catheter is in place, and a cesarean

section becomes urgent, dosing of the epidural with 2-chloroprocaine will
achieve successful block within about 5 minutes. Due to the rapid breakdown
of 2-chloroprocaine by plasma cholinesterase, the duration of action is only
about 45 minutes. Anticipating a prolonged need for analgesia, the anesthesia
provider can preemptively dose the epidural with lidocaine intraoperatively to
extend the length of the neuraxial analgesia. Finally, a plan for post-operative
analgesia needs to be established since epidural opioids following
administration of 2-chloroprocaine are ineffective. It is thought that 2-
chloroprocaine or a metabolite binds to the opioid receptors rendering them
unavailable for subsequent opioid dosing [53].
Both bupivacaine and ropivicaine can be used for epidural anesthesia for
cesarean section. The time to onset, as well as the duration of the anesthetic
makes these two options less desirable when faster onset is needed or quicker
recovery is desired.
The addition of opioids adds a synergistic benefit, improving the quality
of the anesthetic without significant adverse affects to the fetus or the mother.
Fentanyl for intra-operative analgesia or preservative free morphine for post-
operative pain relief has proven to be very efficacious. Careful monitoring of
the maternal respiratory status must be documented since neuraxial morphine
will cause respiratory depression.
Combined spinal epidural (CSE) anesthesia offers the benefit of quick
onset of spinal analgesia with the added benefit of being able to prolong the
anesthetic if needed by an indwelling epidural catheter. Placing a spinal needle
into the touhy needle after a loss of resistance technique has been used to
identify the epidural space employs a needle through needle technique. Once
the spinal dose has been delivered, the epidural space is dilated with a bolus of
saline and the epidural catheter is thread into the epidural space. The patient is
then placed supine in a left uterine displacement tilt and the level of the
blockade is measured. Using a pencil point needle for the spinal dose rather
than a cutting or beveled needle decreases the risk of post-dural puncture
headache [28]. In patients with difficult airways however, caution should be
taken with CSE technique since the function of the epidural catheter cannot be
verified prior to the spinal anesthetic wearing off.
Single shot spinal anesthetics are very common especially if the risk of a
prolonged procedure is very low. Spinal anesthetics offer the benefit of rapid
onset and traditionally faster placement as compared to epidurals. Like all of
the neuraxial procedures where local anesthetics are used, sympathectomy can
lead to maternal hypotension and fetal bradycardia. Maternal hypotension may
be heralded by maternal nausea and vomiting which often times is relieved

when the hypotension is treated.
Whereas epidural dosing is volume driven to achieve a given dermatomal
level of analgesia, spinal dosing is based on the baricity of the local anesthetic
that is used. Baricity refers to the density of the local anesthetic as compared
to the cerebral spinal fluid that the local is injected to, both being compared at
equal temperature. With hyperbaric solutions, the local anesthetics are
prepared in dextrose making them denser as compared to CSF. Isobaric
solutions are of equal density to CSF and finally hypobaric solutions are
diluted in sterile water creating a less dense solution when compared to CSF.
The position of the patient after the spinal anesthetic has been given will
dictate how far the patient will get dermatomal coverage with anesthetists
using either hyperbaric or isobaric solutions for patients having cesarean
sections.
Due to the increased risk of post-dural puncture headaches with cutting-
bevel needles, it is recommended that pencil-point needles like the Whitacre,
Sprotte, or Gertie Marx needles be used for the procedure. Bupivicaine is the
most common spinal local anesthetic that is used with duration of 90-120
minutes. Although lidocaine has been used in the past, due to increased
incidence of transient neurological symptoms (TNS), where the patient
experiences pain in the legs and back for 24-48 hours following the spinal.
Therefore its popularity as a spinal anesthetic has fallen out of favor [54]. Like
epidural analgesia, the addition of opioids to the spinal allows for improved
intraoperative analgesia or post-operative pain control, yet this has to be
balanced with the risk of respiratory depression, pruritis, and nausea and
vomiting.
ANESTHETIC COMPLICATIONS RELATED

TO NEURAXIAL ANALGESIA
As discussed earlier, one of the most common complications of neuraxial

analgesia is the hypotension that results from the sympathectomy after
infiltration of local anesthetic. The subsequent peripheral vasodilation and
venous pooling leads to decreased cardiac return and cardiac output. Most
providers avoid the use of colloid as a prophylactic measure and use a
judicious bolus of crystalloid which may decrease the incidence of
hypotension, yet is unable to reliably prevent it [28].
The use of vasopressors, either phenylephrine or ephedrine, has also been

used when hypotension from neuraxial sympathectomy results. Although both
are acceptable options if hypotension exists, phenylephrine should be the
preferred vasopressor if no evidence of maternal bradycardia since it has been
shown to result in a better umbilical artery blood pH as compared to ephedrine
[55]. However, if maternal bradycardia is a concern, ephedrine is a reasonable
alternative. No consensus has been reached about the use of prophylactic
infusions of phenylephrine. Bolus dosing as compared to continuous infusion
has been shown to use less vasopressor and better blood pressure control in the
first 6 minutes after induction thus leading most anesthesia providers to use the
bolus-dosing regimen [56].
Postdural puncture headache (PDPH) is one cause of post-partum
headache and the incidence of inadvertent postdural puncture varies with the
experience of the practitioner being inversely related to the incidence. The
pathophysiology of the headache is thought to be related to one of two
theories. First it is thought that the loss of CSF allows for the brain to sag thus
causing meningeal traction [57]. This theory is supported by the observation
that PDPH symptoms are significantly worse in the upright position as
compared to the recumbent position. The second theory also relates to the loss
of CSF. Intracranial hypotension leads to a compensatory vasodilation,
causing a migraine-like headache. This theory is supported by MRI images
that show increased cerebral blood flow in PDPH [58].
The majority of postdural puncture headaches occur within 48 hours of the
initial neuraxial procedure. Although a severe positional headache is the most
informative symptom leading to a diagnosis, other symptoms can include
nausea, vomiting, hearing loss, tinnitus, vertigo, scalp paresthesia, visual
disturbances, and cranial nerve palsies. If there was a lack of recognized dural
puncture, caution should be taken to not rule out more nefarious pathology
such as intracranial hemorrhage where a delay in diagnosis could be
catastrophic.
Goals for treating PDPH focus on replacement of the lost CSF, sealing the
puncture site, and controlling the cerebral vasodilation. Conservative
management of postdural puncture headaches includes IV or oral hydration,
abdominal binder, IV or oral caffeine, and analgesics. Although bed rest and
the supine position may decrease the discomfort from the positional headache,
ambulation should not be avoided since bed rest has no impact on the duration
of the headache [59]. If no interaction is taken, the headache is usually self-
limiting with the majority of the headaches spontaneously resolving within
7-10 days after onset. Although most headaches resolve without intervention,
new mothers will often find that the pain prevents them from caring for and
bonding with their child especially after they have been discharged from the
hospital. In these cases, epidural blood patch often provides definitive
treatment in most women receiving the procedure for PDPH.
An initial epidural blood patch has a success rate between 70-98% if it is
performed greater than 24 hours after the initial dural puncture. A subsequent
epidural blood patch also has about the same success rate if the first one failed
to give relief [60]. When placing the blood patch, placing the epidural as close
to the initial interspace allows for a better chance that the therapy will reach
the site of the dural leak. Communication with the patient throughout the
procedure is imperative and if the patient experiences significant back pain
while 15-20 ml of sterile blood is injected, the procedure should be stopped.
Following the procedure, the patient should lay supine for 1-2 hours. Given
that not all patients that have an unintended dural puncture develop a postdural
puncture headache, prophylactic blood patches subject a portion of patients to
undue risk; therefore most providers do not follow this practice.
Local Anesthetic Systemic Toxicity (LAST) is a potentially catastrophic
complication that the anesthesia provider needs to be aware of and monitor for
any time a neuraxial technique is performed. Although a negative test dose
following epidural placement reassures the provider that the epidural catheter
is not intravascular, it does not guarantee that the catheter remains outside of
the intravascular space during the period that the catheter is left indwelling.
LAST begins with neurological and cardiovascular involvement and is often
seen with a period of excitation including tachycardia and seizures followed
by cardiovascular collapse and unconsciousness. Treatment is initially
supportive following advanced cardiac life support (ACLS) protocols in the
case of cardiovascular collapse and airway management. Lipid emulsion
therapy is the definitive treatment of choice and should begin once a suspicion
for local toxicity is high. Care should be taken each time the epidural is bolus
dosed and catheter aspiration should be done to demonstrate no withdrawal of
blood. Fractioned doses (<5ml) should be given of the local if large volume
dosing is needed to allow early recognition of a misplaced or catheter that has
migrated after placement.
High or total spinal blocks may occur after unintentional subarachnoid or
subdural infusion of local anesthetic intended for the epidural space. Epidural
catheters may migrate following prolonged labor and using test dose as well as
aspiration prior to any injections of anesthetics helps decrease the risk of
unintentional intrathecal injections. Since the intrathecal space and the
subdural space are continuous with the brain stem, local anesthetics can
migrate cephalad involving the cranial nerves.
Another potential cause for a high spinal can occur following placement of
a spinal block following a failed or incomplete epidural. In these cases, the
dural sac is compressed by prior epidural dosing thus causing a more cephalad
spread of the spinal agents and subsequently leading to a total or high spinal.61
Some anesthesia providers choose to avoid this potential devastating
complication and decide not attempt a spinal after a failed epidural, other
providers will proceed with a spinal but will pick a different interspace and
modify the amount of the spinal anesthetic that is used.
When high doses of local anesthetics are infused into the epidural space
they will not spread intra-cranially, however they can still spread cephalad
enough to cause respiratory arrest and affect the cardiac accelerator fibers that
lie between T1-T4 leading to bradycardia in the face of hypotension following
sympathectomy. If a patient continues to have respiratory distress and
hypotension, the anesthetic should be transitioned to general anesthesia and
resuscitative efforts including vasopressors, and ACLS implemented as
needed. If the patient has a high level yet is still maintaining adequate
oxygenation and ventilation as indicated by visualization of chest rise, oxygen
saturation, and end-tidal CO2, then reassurance for the patient, and
supplemental oxygen are needed; with increased vigilance for further
respiratory and cardiovascular compromise if the neuraxial level continues to
rise. In cases of cardiovascular collapse following total spinal blockade, IV
epinephrine (1mg) is necessary as well as resuscitation by ACLS protocol.
Cases of failed or incomplete analgesia coverage from an epidural have an
occurrence ranging from 2% failed to 15% of inadequate analgesia [62]. The
risk of catheter migration increases as the length of time that the parturient has
the indwelling catheter. In cases of one-sided epidural, pulling back the
catheter a centimeter or two so that the catheter depth is not greater than 6 cm
may help rescue a one sided epidural. Placing the patient in a lateral position
so that the painful side is in the dependent position may help once the catheter
position has been confirmed and migration of the catheter has been excluded.
Ensuring adequate spread of the local anesthetic by using 5-10ml of dilute
(bupivacaine 0.0625% to 0.125%) can often allow increased coverage in areas
where inadequate analgesia are noted. If a laboring woman is unable to get any
significant relief, the provider can choose to dose the catheter with 5ml of 2%
lidocaine with bicarbonate and reevaluate the block after 10 minutes. If the
parturient is getting no pain relief, the catheter should be immediately removed
and replaced if the patient allows. The addition of opioid to the epidural local
infiltration can occasionally provide increased patient satisfaction if there are

segments that were incompletely covered or missed entirely.
Parturients that request spinal analgesia after identification of a failed
epidural catheter should be approached with extreme caution. The risk of a
high neuraxial block is of concern and the safest approach to these patients
would be replacing the epidural catheter without penetrating the subarachnoid
space, or general anesthesia in cases of emergent cesarean section.
Maternal obesity can complicate all aspects of care for the obstetrician and
the anesthesiologist and an interdisciplinary approach has to be taken for the
successful management of this growing patient population. It is estimated that
more than 1/3 of Americans (34.9% or 76.8 million) are obese [63]. In the
parturient, obesity has to be a factor when considering management
considering that in the 2000-2002 Confidential Enquiries into Maternal Death
and Child Health, 35% of all parturients who died were obese [64]. Obesity is
rarely a disease exclusive of other co-morbidities. More often, other
pathologies including diabetes, hypertension, cardiovascular disease,
restrictive lung disease, obstructive sleep apnea and fatty liver disease further
contribute to increased morbidity and mortality.
Some obstetric complications are more common in the obese patient
population such as increased risk of cesarean delivery, preeclampsia and
chronic hypertension, fetal malpresentation, postdates pregnancy, and
postpartum hemorrhage. Anesthetic complications related to patient obesity
such as technical difficulty in placing neuraxial blocks, increased risk of
epidural catheter migration, increased airway complications including
difficulty with both intubation and ventilation and increased risk of aspiration
further complicate the management within this patient population.
In the obese population there has to be a high motivation for neuraxial
anesthesia if there is any concern of difficult airway. Although many obese
parturients are able to labor successfully, as BMI increases, the risk of
cesarean delivery becomes more likely [65]. The longer an indwelling epidural
catheter remains, the higher the probability that the catheter will migrate thus
preventing effective analgesia for labor and more importantly, the less reliable
it becomes if needed for an emergent or urgent cesarean section. After an
epidural is placed, vigilant assessment of the catheter will alert the anesthesia
provider of a poorly or non-functioning neuraxial catheter. In cases of
anticipated difficult intubation and where difficulty in placing a labor epidural
is encountered, consideration of placing an intrathecal catheter should be
weighed.
In cases where general anesthesia is indicated, such as an emergent

procedure or a contraindication for a neuraxial block, airway considerations
and aspiration have to be paramount in planning the anesthetic. Patient
positioning with a ramp under the patient’s upper back and leading up to the
occiput allows for better alignment of the patient’s oral axis, laryngeal axis,
and pharyngeal axis. Having additional equipment such as oral airways,
Glidescope, laryngeal mask airways, and personnel available increase the
likelihood of successful airway management. As stated earlier, with a patient
with a known or suspected difficult airway, awake fiberoptic intubation is the
safest option.
Prior to induction of general anesthesia, adequate pre-oxygenation is
extremely important in the obese pregnant patient. The increased oxygen
needed by the fetus as well as increased oxygen consumption in the obese
patient make significant desaturation after induction very common. Decreased
functional residual capacity due to pregnancy, obesity and the supine position
make the amount of reserve available prior to desaturation very small. Taking
time to get adequate pre-oxygenation with 100% oxygen by a tight fitting
facemask for three minutes prior to induction gives the anesthesia provider the
best opportunity to avoid respiratory compromise.
The risk of pulmonary aspiration under general anesthesia is further
increased in the morbidly obese population. Although there is conflicting
evidence as to whether or not the obese patient has increased gastric volume or
decreased gastric pH, it is clear that the incidence of hiatal hernia and reflux is
increased in this population making the risk of aspiration very concrete.
Although the American Society of Anesthesiologists has issued a practice
guideline for dictating NPO guidelines, they clearly state that these guidelines
are intended for healthy patients of all ages however they exclude laboring
parturients [66]. Since no clear guidelines are available for laboring obese
parturients, strict NPO standards should be employed and evaluated on a case-
by- case basis with the ASA guidelines as the most minimum standard. Use of
a non-particulate antacid is also required. The use of cricoid pressure is also
recommended although some argue its efficacy given some research showing
that the use of cricoid pressure decreases the lower esophageal sphincter tone
and can potentially make visualization during intubation more
difficult [67, 68].
Advanced maternal age (AMA), where the woman will give birth at the
age over 35 years is a growing trend in developed countries. A fourfold
increase in maternal mortality when the mother is over 35 years as well as
increased risk of developing complications during the pregnancy make this

patient population complicated [69].
Pregnancies in the AMA patient are often complicated by multiple
gestation, although IVF contributes to this, the risk of twin gestation is higher
even in patients that have not had IVF. In a parturient over the age of 35 years
old, who has had 4 or more children, she is 3 times more likely to have a twin
gestation than a 20-year-old female without children [70].
The AMA parturient is also at increased risk of gestational diabetes
mellitus. This increased risk is related to the decrease in pancreatic B cell
function and decreased insulin sensitivity with increased age. Preeclampsia,
gestational hypertension, miscarriage, small for gestational age, large for
gestational age, spontaneous preterm delivery, and increase incidence of
cesarean delivery is also increased within this population. Evidence does not
show an increase in uterine bleeding or placental abruption in advanced
maternal age patients however there is a nine fold increased risk of placenta
previa in patients older than 40 years as compared to patients at age 20 [71].
With current obstetric and anesthetic management, these patients can be
successfully managed.
Hypertensive disorders of pregnancy including gestational hypertension,
chronic hypertension, preeclampsia, eclampsia, and HELLP are some of the
leading causes maternal mortality particularly in the developed world and
affect about 10% of all pregnancies worldwide [72]. Complications stemming
from these hypertensive urgencies include: cerebrovascular accident,
pulmonary edema, renal failure, and placental abruption. Preeclampsia is
defined as the onset of hypertension in a pregnancy after 20 weeks gestation
with proteinuria in a previously normotensive parturient. Severe features of
preeclampsia include any of the following:
 Systolic blood pressure of 160mm Hg or higher, or diastolic blood

pressure of 110mm Hg or higher on 2 occasions at least 6 hours apart
on bed rest
 Thrombocytopenia (platelet count less than 100,000/microliter) or
Impaired liver function or Fetal growth restriction
 Oliguria <500 mL in 24 hours
 Proteinuria ≥5g in a 24 hour urine specimen or ≥3+ on 2 random urine
samples collected at least 4 hours apart
 Cerebral or visual symptoms
 Pulmonary edema or cyanosis
 Epigastric or right upper quadrant pain
Preeclampsia can also occur up to 6 weeks post-partum. Delivery is the

definitive treatment of preeclampsia with goals prior to delivery being blood
pressure management and prevention of seizure. Timing of the delivery is
complicated by the gestational age of the fetus, and the severity of the disease.
Eclampsia is the onset of seizures in a parturient with preeclampsia. 80%
of the cases of eclampsia occur intrapartum or within the first 48 hours after
delivery. However a seizure can occur as late as 2 weeks after delivery [73].
Each seizure generally lasts between 60-75 seconds with further complications
of the seizure including tongue biting, aspiration and head injury.
Obstetric management includes the use of antihypertensive medications as
well as anticonvulsants, most commonly used in the United States is
magnesium sulfate. Magnesium sulfate works in a multifactorial fashion by
causing neural stabilization, stabilization of the blood brain barrier, and
decreased cerebral edema formation. Although magnesium sulfate also
contributes to peripheral vasodilation, other antihypertensive medications such
as labetalol, hydralazine, nifedipine are more effective for blood pressure
management. Nitroglycerine and sodium nitroprusside are reserved for
intractable hypertension and acute hypertensive crisis.
Magnesium sulfate has a narrow therapeutic range (4-8 mEq per L) and
levels higher than this can lead to decreased deep tendon reflexes, respiratory
depression, ECG changes and cardiac arrest. Magnesium sulfate also prolongs
the duration of depolarizing and non-depolarizing muscle relaxants due to the
inhibition of acetylcholine release.
HELLP Syndrome (Hemolysis Elevated Liver enzymes Low Platelets)
occurs in approximately 1 in 1000 pregnancies [74]. Although it is categorized
as a subset of severe preeclampsia in some of the patients they do not have
hypertension or proteinuria. Parturients with HELLP syndrome are managed
with delivery being imminent, with delay only being for a short period to
initiate steroid therapy for fetal lung maturity.
Due to the precipitous decline in platelet count that can accompany
preeclampsia and especially HELLP syndrome, initiation of neuraxial
anesthesia early in the patient’s management is imperative given no
contraindications. Although there is not a specific cutoff for minimum platelet
values, most anesthesia providers would consider placing a neuraxial block if
platelet counts were greater than 80,000/mm3. Because platelet value can drop
very quickly, it is prudent to obtain platelet values immediately prior to
placing a neuraxial catheter or block, or removing a neuraxial catheter.
Anesthetic management of the parturient with hypertensive disorders,

specifically preeclampsia takes good communication with the obstetric team.
In addition to platelet count, further investigation of coagulation might be
warranted. Platelet function evaluation by a PFA-100 test or
thromboelastogram (TEG) might be useful however they are infrequently
necessary if neuraxial anesthesia is administered early when platelet count is
still above 100,000 mm3.
If cesarean section is planned for the delivery and a working indwelling
catheter is in place, it can easily be converted for anesthesia for the surgery. If
a catheter is not working or contraindicated, general anesthesia is initiated
after the obstetric team is ready with gown and gloves donned and the patient
prepped. Extreme caution has to be taken with both the patient’s blood
pressure during tracheal intubation, as well as management of a difficult
airway if airway edema is present as a result of the preeclampsia or HELLP
syndrome. In patients who have time for a neuraxial anesthetic and there is no
coagulopathy, either a spinal anesthetic or an epidural can be considered. If a
patient becomes hypotensive due to the sympathectomy from the neuraxial
block, vasopressors can be used judiciously since patients with preeclampsia
may have increased sensitivity to vasopressors [75]. In patients where the
blood pressure ranges have been severe or labile, consideration of a radial
arterial line should be made.
For patients that have been on magnesium sulfate for seizure prophylaxis,
it should remain on throughout the duration of the surgery and into the
postpartum period. For the anesthesia provider, if non-depolarizing muscle
relaxants are used, their duration can be prolonged and their effects should be
monitored with a nerve stimulator. Also of concern is the increased risk of
uterine atony following delivery of the neonate. Uterotonic agents should be
immediately available as in any cesarean delivery.
Postpartum hemorrhage is defined as the loss of more than 500ml of blood
in a vaginal delivery and more than 1000ml in a cesarean section. Worldwide
postpartum hemorrhage is the leading cause of maternal mortality. Postpartum
hemorrhage is further divided into primary, being within the first 24 hours
from delivery and secondary, occurring 24 hours to 6 weeks postpartum.
Although uterine atony is the most common cause, other contributors include
lacerations, uterine rupture, retained products and placenta accreta.
At term, cardiac output to the uterus is increased to 10-20% allowing an
atonic uterus to lose up to 2 L of blood within a few minutes [76]. Uterine
massage and oxytocin are the initial agents used to combat the atony that
ensues after delivery. 20-50 Units is added to a 1 liter bag of crystalloid with
avoidance of bolus dosing due to the risk of hypotension since oxytocin is a

vasodilator. A second line agent is ergot alkaloids, which cause
vasoconstriction, and increased uterine tone thus they are relatively
contraindicated in hypertensive patients such has those with preeclampsia or
gestational hypertension. Prostaglandins can be used if other agents have
failed or are contraindicated. IM dosing every 15 minutes for a total of 2mg
can be used. These agents should be avoided in patients with a history of
asthma. Prostaglandins have been shown to cause increased
bronchoconstriction leading to abnormal ventilation-perfusion ratios and
hypoxemia. Finally, misoprostol can be considered with few side effects yet a
slower onset of action as compared to the other agents.
If post-partum hemorrhage due to uterine atony continues, more invasive
actions must be considered with an interdisciplinary approach leading to the
greatest success. Obstetricians need to quickly coordinate with nurses,
anesthesia providers, interventional radiologists, blood bank pathologists, and
other obstetricians with rapid advancement through increased invasive
management strategies such as tamponade techniques, surgical compression or
arterial ligation, radiological arterial embolization, and ultimately
hysterectomy if hemorrhage remains uncontrolled with less definitive
treatments. Anesthesia providers need to obtain peripheral access or central
access if large bore IVs are unavailable. Blood banks need to initiate massive
transfusion protocols if available. If hospitals do not have access to large
volume blood bank resources, plans for transfer have to be initiated. Labs
including ACT, hemogram, coagulation studies, electrolytes have to be
trended and used to help dictate the resuscitative efforts.
In cases of retained placenta, anesthetic management depends on the
presence or absence of hemorrhage as well as how stable the patient is. If the
patient has an indwelling epidural catheter and there is little to no hemorrhage,
dosing of the catheter to provide analgesia while the retained products are
retrieved offers the easiest option. If no catheter is available or if there is
enough hemorrhage to warrant prevention of further sympathectomy, cautious
use of IV analgesics such as fentanyl, remifentanil, or ketamine can be
considered. However extreme caution has to be taken so that the maternal
respiratory effort is maintained and airway reflexes are not lost. In cases of
extreme hemorrhage indicated by massive transfusion and maternal instability,
general anesthesia has to be the choice to avoid sympathectomy and further
hypotension.
Another leading cause of maternal hemorrhage is placental accreta.
Placenta accreta is when the placenta abnormally invades the uterus thus
preventing separation. If the placenta invades into the myometrial wall this
type of accreta is categorized as a placenta increta. If the placenta invades
beyond the myometrium and into the serosa or into other adjacent tissues such
as the bladder, this is referred to as placenta percreta. Preparation for this
complication by both the obstetrician as well as the anesthesia provider allow
for the best patient management with less morbidity and mortality, thus
antenatal diagnosis is ideal. In most cases placenta accreta is first identified on
prenatal ultrasound, yet if the ultrasound is equivocal, prenatal MRI is used.
Management of a placenta accreta is driven by the enormous risk of
hemorrhage. In known cases of accreta, most obstetricians plan for scheduled
cesarean delivery with hysterectomy based on American Congress of
Obstetricians and Gynecologists (ACOG) guidelines. In these cases, care is
taken to not disturb the placenta once the neonate is delivered. The uterus and
placenta are then surgically removed thus decreasing the amount of surgical
bleed and avoiding manipulation of the placenta and uterine interface where
hemorrhage is most likely to stem from.
If the diagnosis of placenta accreta is unclear, an obstetrician may choose
to wait on a hysterectomy and see if the release of the placenta clarifies that
placenta accreta was not the pathology. If the obstetrician chooses to wait for
placental release, the obstetrician has to resist manually pulling the placenta
off of the uterine wall thus initiating hemorrhage.
Planning for a scheduled cesarean section in cases of known or suspected
placenta accreta includes planning for resuscitation with blood products if
there are no contraindications such as patient refusal. In most routine
deliveries, there is no need for blood type and cross-match, however in cases
where large blood loss is anticipated, it is imperative to have the blood bank
type and cross for multiple units. In small community hospitals where blood
bank supplies are limited planning on transfer to a larger facility might offer
the safest option if massive resuscitation is needed. Large bore IV access also
has to be attained prior to surgical delivery. Invasive blood pressure
monitoring with an arterial line should be considered and in the most
conservative strategies would be employed to help follow not only blood
pressures, but resuscitative efforts via blood gas values. The need for central
access offers little benefit if large bore peripheral access is obtained. If
vasoactive medications are used for management of hemodynamics in cases of
severe massive hemorrhage, a central line can be of benefit.
When planning the type of anesthesia used, discussions with the patient as
well as the obstetrician are imperative so that the safest plan can be executed
with the patient and obstetrician supporting the plan. If there is concern of
placenta percreta, general anesthesia offers the benefit of avoiding a

sympathectomy from neuraxial anesthesia, it also avoids the discomfort of
prolonged immobility if delicate yet lengthy dissections are required. In some
cases, if the dissection exceeds the level of the surgical intervention including
retraction, neuraxial anesthesia might have to be converted to general
anesthesia intraoperatively. If there is a low risk of accreta, the option of
beginning the case under neuraxial anesthesia then converting to a planned
general anesthetic after the delivery of the neonate is an option. The benefit
being allowing the mother to participate in her delivery, yet the downside is
the sympathectomy that can lead to further blood loss in a hemorrhage. Thus,
the most conservative management would be for planning of a general
anesthetic with the obstetric team bedside and ready for delivery of the
neonate immediately after induction and the airway is secured.
Another obstetric complication that requires prenatal planning is placenta
previa. Normally implantation of the placenta occurs in the upper uterine
segment, however in placenta previa the placenta implants over or near the
internal cervical os. A complete placenta is when the placenta completely
covers the cervical os. A partial previa occurs when the cervix is partially
covered. Marginal previa is diagnosed when the placenta is adjacent to the
internal os, yet it does not cover the opening. A low-lying placenta is when
implantation occurs in the lower uterine segment, rather than in the upper
uterine segment. When painless bleeding occurs in the second or third
trimester, diagnosis of placenta previa has to be made until ruled out by
ultrasound. When placenta previa is known antenatally, elective cesarean
section is scheduled. If bleeding is complicating the pregnancy, and efforts to
stop the bleeding such as bed rest or tocolytics fail, an urgent cesarean section
is planned with knowledge of pre-operative hemoglobin and hematocrit. If
preoperative anemia is significant, a type and cross is necessary with plans for
resuscitation if further intraoperative blood loss compromises the patient’s
clinical stability. If the patient is pre-term and the bleeding has abated, the
patient may continue the pregnancy with bed rest allowing for continued fetal
growth and maturity.
As in other cases of maternal bleeding or risk of hemorrhage, the
anesthetic plan is dictated by the urgency of the cesarean section, pre-operative
stability, degree of pre-operative anemia, and concern of maternal difficult
airway. If the patient has been hemodynamically stable and there is time for
neuraxial anesthesia, epidural allows for avoidance of risks of general
anesthesia specifically risk of aspiration and risk of failed airway. The benefit
of general anesthesia allows for avoiding a sympathectomy in a patient who
might be volume depleted due to pre-operative vaginal bleeding. The choice of

anesthetic is determined on an individual basis with the risks and benefits of
each considered.
In patients with placenta previa, a high index of suspicion for placenta
accreta is needed particularly if the patient has had previous cesarean sections.
As the number of previous cesarean sections increase, a correlation exists with
an increased risk of placenta accreta if the patient also has a placenta previa.
For patients with placenta previa and no prior cesarean sections, the risk of
placenta accreta is 3%. If the patient has had one prior section, the risk
increases to 11%. If two prior sections, the risk is 40%, and the risk rises to
greater than 60% if the patient has had three or more prior sections and a
current previa [77]. In these cases, prenatal screening offers the benefit of
careful interdisciplinary planning of a scheduled cesarean section to decrease
the risk of hemorrhage.
Premature separation of the placenta from the decidua basalis is referred to
as placental abruption and can compromise the fetus as well as mask maternal
hemorrhage behind the abruption. Abruption can occur after 20 weeks
gestation and the most common signs are vaginal bleeding with abdominal or
uterine pain, uterine contractions and a nonreassuring fetal heart rate may also
be present. It is important to realize that in 20% of cases of abruption, vaginal
bleeding will not occur [78].
Some risk factors for uterine rupture include history of previous abruption,
abdominal trauma, advanced maternal age, premature rupture of membranes,
congenital uterine abnormalities, hypertensive disorders, and maternal cocaine
abuse. If a patient has vaginal bleeding especially in the setting of abdominal
pain and contractions, concern for abruption needs to be investigated initially
with ultrasound which can be very specific yet not very sensitive. Although
MRI can detect missed abruptions from ultrasound, there is little justification
for this testing given minimal changes in patient care if an abruption is
verified.
Management of the patient with placental abruption takes into
consideration multiple factors including, maternal stability, fetal heart tracing,
gestational age of the fetus, and chronic versus acute bleed. Initial
management of the parturient regardless of these factors include, fetal
monitoring, establishment of large bore peripheral IV access, type and cross
match, initial lab values including hematocrit and coagulation status. If the
patient is stable and the abruption is not compromising fetal well-being, the
decision by the obstetric team may include delaying delivery for the benefit of
increasing the fetal gestational age. If this plan is implemented, vigilant
monitoring of the maternal and fetal well-being is necessary given that the size
of the abruption can acutely increase leading to fetal demise and maternal
hemorrhage. If on initial presentation, the fetus or parturient are unstable, the
decision for delivery allows for definitive treatment.
The mode of delivery is also dependent on the acuity of the situation. If
both the mother and fetus are stable, vaginal delivery is the preferred option. If
emergency cesarean delivery is necessary, general anesthesia usually allows
for the quickest anesthetic weighed against the risks of aspiration and difficult
airway. If the cesarean section is urgent yet time for neuraxial anesthesia is
available, further thought has to be given to the sympathectomy and the
amount of vaginal bleed or concealed bleed behind the placenta. If there is any
concern of coagulopathy, or hemodynamic instability, general anesthesia
offers the safest option.
Volume resuscitation should be goal directed following clinical signs of
tachycardia and hypotension. The need for invasive blood pressure monitoring
may be necessary if the amount of bleed from the abruption is large, thus
allowing for further markers such as pH, lactate, base deficit and hematocrit to
dictate resuscitation.
Vasa previa is another maternal complication that necessitates close
maternal monitoring and a planned cesarean delivery. Vasa previa occurs
when the fetal blood vessels are contained within the membranes that cover
the cervical os. Unlike a placental abruption where both the mother and fetus
are at significant risk if hemorrhage ensues, the fetus bares the largest risk if
there is rupture of membranes and a vasa previa exists. If membranes rupture
the risk of fetal death is high from fetal exsanguination or fetal asphyxia as
components of the fetal vessels are compressed compromising blood flow to
the fetus.
The highest success for survival of the fetus is a planned cesarean section
between 34 and 35 weeks gestation [79]. This timing allows for a balance
between allowing for increased fetal maturity with a decreased risk of
premature rupture of membranes. As long as there are no contraindications for
a neuraxial technique, this should be the anesthetic of choice. Although
general anesthesia can be considered, there is no increased benefit from a
planned general anesthetic in a scheduled cesarean section. If a patient
presents with fetal distress and membranes are ruptured, general anesthesia is
the preferred method due to the benefit of decreased time to delivery.
Amniotic fluid embolism (AFE) is a complication that can occur during
any trimester of the pregnancy although it is most common during labor. Since
amniotic fluid embolism is a diagnosis of exclusion and reporting is often
incomplete, understanding the mortality associated with AFE is broad with

estimates between 20%-80%. Even if the mother survives the incident,
neurologic injury is common and ranges from short-term memory loss to
complete anoxic brain injury. Mortality to the fetus is also high ranging from
20%-60% [80].
Unlike a mechanical obstruction of blood flow in profound air embolism,
AFE is thought to be a humoral response with a release of endogenous
inflammatory mediators. This cascade of thromboxane, prostaglandins,
leukotrienes, and endothelins leads to a biphasic response. The initial
presentation usually involves one or more of the following: shortness of
breath, hypotension, anxiety or agitation, DIC, fetal distress, or seizures.
During this initial phase, inflammatory mediators cause pulmonary vasospasm,
severe hypoxia, and subsequent right-sided heart failure. If bedside cardiac
echo is done during this phase, a dilated right ventricle will be indicative of
severe pulmonary hypertension. The late phase of amniotic fluid embolism
occurs about 30 minutes after the initial insult and is lead by left sided heart
failure with cardiac output being significantly decreased concurrent with
pulmonary edema and decreased systemic vascular resistance.
Although the symptoms of amniotic fluid embolism encompass a large
differential diagnosis, the initial management is the same regardless of the
cause. Supportive efforts with maternal ACLS, airway management with
intubation, and following coagulation abnormalities while correcting with
blood products allows for the highest rate of maternal and fetal survival.
Invasive lines such as an arterial line and central venous access for the
delivery of massive transfusion in cases of DIC, or vasopressors in
cardiovascular collapse should be placed early to help in the resuscitation.
Cardiovascular collapse in pregnancy regardless of the gestational age can
be devastating with the loss of two lives being in the forefront of most
providers’ thoughts and efforts in resuscitation. Little changes in the ACLS
protocols are made for the parturient. In patients with a gravid uterus beyond
20 weeks of gestation or where the uterus is at or above the level of the
umbilicus then left uterine displacement should be implemented during the
chest compressions. Trying to relieve the uterocaval compression to allow
cardiac preload to return to the heart can also be accomplished by having an
individual pull the gravid uterus the patient’s left side thus relieving the
resistance to cardiac preload. The benefit to this technique allows the patient to
remain supine for easier and more effective chest compressions and better
access to airway management. Chest compressions should be done with hand
positioning unchanged from a non-pregnant patient according to the 2015
American Heart Association ACLS guidelines with approximately 100 high

quality compressions per minute allowing for adequate recoil in between
compressions [81]. Energy requirements for defibrillation and medications and
doses remain unchanged in the pregnant patient as compared to the non-
pregnant patient.
In patients who have a gravid uterus beyond 20 weeks gestation who is in
cardiovascular collapse requiring ACLS, the decision for a perimortem
cesarean section has to be considered and interdisciplinary efforts for delivery
coordinated. Anoxic brain injury has been shown after 4 minutes after
identification of cardiovascular collapse requiring chest compressions. The
best chance of survival for both the fetus as well as the mother is the 4/5 rule.
Within four minutes of initiation of CPR and cardiac arrest, a plan for infant
delivery should be made and by five minutes, the delivery complete [82]. At
that point after delivery, uterocaval compression has been completely relieved
and the patient has the best chance for return of spontaneous circulation.
During the cesarean section, ACLS should not be interrupted and the two
should occur simultaneously with high quality chest compressions being
imperative for the best chance for the fetus to survive. Having a plan for fetal
delivery by five minutes after maternal cardiovascular collapse is ideal,
however, a delay in fetal delivery should not prevent the efforts since studies
have shown fetal survival and even normal infants have been delivered after
30 minutes after maternal arrest [82]. If maternal arrest occurs while in the
labor hall while she was laboring, then the need to wait 5 minutes for return of
maternal spontaneous circulation is not necessary. Delivery should occur
immediately since the obstetrician was already planning on delivery and the
gestational age is appropriate for delivery.
REFERENCES
[1] Gin T, Chan MT. Decreased minimum alveolar concentration of
Isoflurane in pregnant humans. Anesthesiology 1994; 81: 829-32.
[2] Chan MT, Mainland P, Gin T. Minimum alveolar concentration of
halothane and enflurane are decreased in early pregnancy.
Anesthesiology 1996; 85:782-6.
[3] Chan MT, Gin T. Postpartum changes in the minimum alveolar
concentration of isoflurane. Anesthesiology 1995; 1360-63.
[4] Sharrock NE, Greenidge J Epidural dose responses in pregnant and non-
pregnant patients, Anesthesiology 1979, Vol 51 (Supplement), S299.
[5] Teoh WHL, Ithnin F, Sia ATH, Comparison of an equal-dose spinal

anesthetic for cesarean section and for post-partum tubal ligation.
International Journal of Obstetric Anesthesia, July 2008; 17:228-232.
[6] Conrad Kirk P. Maternal vasodilation in pregnancy: the emerging role of
relaxin. American Journal of Physiology, August 2011; 301:R267-275.
[7] Ylikorala O, Jouppila P, Kirkinen P, et al. Prostacyclin production
during pregnancy: comparison of production during normal pregnancy
and pregnancy complicated by hypertension. Am J Obstet Gynecol
1982:142:817-822.
[8] Robson SC, Hunter S, Boys RJ, Dunlop W. Serial study of factors
influencing changes in cadiac output during human pregnancy. Am J
Physiol 1989; 256:H1060-5.
[9] Spatling L, Fallenstein F, Huch A, et al. The variability of
cardiopulmonary adaption to pregnancy at rest and during exercise. Br J
Obstet Gynaecol 1992; 99(suppl 8):1-40.
[10] Bernstein IM, Ziegler W, Badger GJ. Plasma volume expansion in early
pregnancy. Obstet Gynecol 2001; 97:669-72.
[11] Lumbers ER, Pringle KG. Roles of the circulating renin-angiotensin-
aldosterone system in human pregnancy. American J of Physiology
2014; 306:R91-101.
[12] Recommendations to prevent and control iron deficiency in the United
States. Centers for disease control and prevention. MMWR Recomm Rep.
1998;47:1-29.
[13] Franchini M. Haemostasis and pregnancy. Thromb Haemost.
2006;95:401-413.
[14] Rajasekhar A, Gernsheineer T, Stasi R, James AH. 2013 Clinical
practice guide on thrombocytopenia in pregnancy a quick reference
presented by the American Society of Hematology.
[15] Gernsheimer T, James AH, Stasi R. How I treat thrombocytopenia in
pregnancy. Blood 2013; 121 (1):38-47.
[16] Higuchi H, Yakagi S, Zhang K, Furui I, Ozaki M. Effect of lateral tilt
angle on the volume of the abdominal aorta and IVC in pregnant and
nonpregnant women determined by MRI. Anesthesiology 2015; 122:
286-93.
[17] Goldsmith LT, Weiss G, Steinetz BG. Relaxin and its role in pregnancy.
Endocrinol Metab Clin North Am 1995; 24:171-86.
[18] Wong CA, McCarthy RJ, Fitzgerald PC, et al. Gastric emptying of water
in obese pregnant women at tem. Anesth Analg. 2007;105:751-55.
[19] Shah S, Nathan L, Singh R, et al. E2 and not P4 increases NO release

from NANC nerves of the gastrointestinal tract: Implications in
pregnancy. Am J Physiol Regul Integr Comp Physiol. 2001;280:R1546-
R1554.
[20] Fister RS, Roberts GS, Grabowski CJ, Cohen S. Inhibition of lower
esophageal sphincter circular muscle by female sex hormones. Amer J of
Physiology-Endocrinology and Metabolism. March 1978; 234(3).
[21] Davison JM, Hytten FE. Glomerular filtration during and after
pregnancy. J Obstet Gynaecol Br Commonw 1974; 81:588-95.
[22] Cheung KL, LaFayette R Renal physiology of pregnancy. Advanced
Chronic Kidney Dis. May 2013; 20(3):209-14.
[23] Dafnis E, Sabatini S. The effect of pregnancy on renal function:
Physiology and pathophysiology. Am J Med Sci 1992;303:184-205.
[24] Berkley KJ, Robbins A, Sato Y. Functional differences between afferent
fibers in the hypogastric and pelvic nerves innervating female
reproductive organs in the rat. Jour Neurophysiol 1993; 69:533-44.
[25] ACOG committee opinion, No 339: Analgesia and cesarean delivery
rates. Obstetrics and Gynecology. June 2006; 107(6) 1487-8.
[26] Osterman M, Martin JA Epidural and spinal anesthesia use during
labor:27 state reporting area, 2008. National vital statistics report from
the Centers for Disease Control and Prevention, National Center for
Health Statistics Vol 59(5):1-13,16.
[27] Berlin Y, Bodian CA, Haddad E, Leibowitz A. Practice patterns of
anesthesiologists regarding situations in obstetric anesthesia where
clinical management is controversial. Anesthesia & Analgesia, 1996;
83(4)735-41.
[28] Practice Guidelines for Obstetric Anesthesia: An Updated Report by the
American Society of Anesthesiologists Task Force on Obstetric
Anesthesia and the Society for Obstetric Anesthesia and Perinatology.
Anesthesiology, 2016; 124(2):270-300.
[29] Peralta F, Higgins, N, Lange E, Wong C, McCarthy R. The relationship
of body mass index with the incidence of postdural puncture headache in
parturients. Anesthesia & Analgesia. August 2015; 121(2):451-56.
[30] Faure E, Moreno R, Thisted R. Incidence of postdural puncture
headache in morbidly obese parturients. Reg Anesth, 1994;19:361-3.
[31] Miu M, Paech MJ, Nathan E. The relationship between body mass index
and post-dural puncture headache in obstetric patients. Int J Obstet
Anesth, 2014;23:371-5.
[32] Rosen, MA. Nitrous oxide for relief of labor pain: A systemic review.
American J of Obstet and Gynecol. 2002;186(5):110-26.
[33] Griffin RP, Reynolds F. Maternal hypoxemia during labor and delivery:
The influence of analgesia and effect on neonatal outcome. Anesthesia
1995;50:151-56.
[34] Yeo ST, Holdcroft A, Yentis SM, et al. Analgesia with sevoflurane
during labor: II. Sevoflurane compared with Entonoxfor analgesia. Br
Jour Anaesth. 2007;98:110-15.
[35] Kuhnert BR, Linn PL, Kennard MJ, et al. Effect of low doses of
meperidine on neonatal behavior. Anesthesia & Analgesia 1985; 64:
335-42.
[36] Hill JB, Alexander JM, Sharma SK, McIntyre DD, Leveno KJ. A
comparison of the effects of epidural & meperidine analgesia during
labor on fetal heart rate. Obstet Gynecol. 2003;102(2):333-37.
[37] Kuhnert BR, Kuhnert PM, Tu AS, Lin DC. Meperidine and
normeperidine levels following meperidine administration during labor.
Am J Obstet Gynecol 1979;133:909-14.
[38] Tsui M, Ngan Kee WD, Ng FF, et al. A double blind randomized
placebo-controlled study of intramuscular pethidine for pain relief in the
first stage of labor. Br J Obst Gyn. 2004;111:648-55.
[39] Olofsson C, Ekblom A, Ekman-Oderberg G, et al. Lack of analgesic
effect of systemically administered morphineor pethidine on labor pain.
Br J Obstet Gynaecol 1996; 103:968-72.
[40] Olofsson C, Ekblom A, Ekman-Ordeberg G, et al. Analgesic efficacy of
intravenous morphine in labour pain: A reappraisal. Int J Obstet Anesth.
1996; 5:176-80.
[41] Gerdine E, Rane A, Lindberg B. Transplacental transfer of morphine in
man. Journal of Perinat Med 1990; 18:305-12.
[42] Maduska AL, Hajghassemali M. A double blind comparison of
butorphanol and meperidine in labor: Maternal pain relief and effect on
the newborn. Can Anaesth Soc J 1978; 25:398-404.
[43] Nicolle E, Devillier P, Delaney B, et al. Threapeutic monitoring of
nalbuphine: Transplacental transfer and estimated pharmacokinetics in
the neonate. Eur J Clin Pharmacol 1996; 49:485-9.
[44] Craft JB, Coaldrake LA, Bolan JC, et al. Placental passage and uterine
effects of fentanyl. Anesthesia & Analgesia 1983; 62:894-98.
[45] Rayburn WF, Smith CV, Parriott JE, et al. Randomized comparison of
meperidine and fentanyl during labor. Obstet and Gynecol 1989; 74:
604-6.
[46] Morley-Forster PK, Reid JW, Vandeberghe H. A comparison of patient-

controlled analgesic fentanyl and alfentanil for labor analgesia. Can J
Anaesth 2000; 47:113-9.
[47] Waring J, Mahboobi SK, Tyagaraj K et al. Use of remifenanil for labor
analgesia: The good and the bad. Anesth Analg 2007; 104:1616-17.
[48] Djabatey EA, Barday PM. Difficult and failed intubation in 3430
obstetric general anaesthetics. Anesthesia. Nov 2009; 64(11):1168-71.
[49] Rose DK, Cohen MM. The airway:Problems and predictions in 18,500
patients. Can J Anaesth. May 1994;41:372-83.
[50] Bontonnet M, Faitot V, Katz A, Salomon L, Keita H. Mallampati class
changes during pregnancy, labour, and after delivery: Can these changes
be predicted? British J of Anaesth. 2010; 104(1):66-70.
[51] Mendelson CL, The aspiration of stomach contents into the lungs during
obstetric anesthesia. Amer J Obstet Gynecol. 1946; 52:191-205.
[52] Tjeuw MTB, Yao F, Van Poznak. Depressant effects of anesthetics on
isolated human gravid and non-gravid uterine muscle. Chin Med J
1986;9:235-42.
[53] Camann WR, Hartigan PM, Gilbertson LI, et al. Chloroprocaine
antagonism of epidural opioid analgesia: A receptor-specific
phenomenon? Anesthesiology 1990; 73:860-3
[54] Fenerty J, Sonner J, Sakur S, Drasner K. Transient radicular pain
following spinal anesthesia: Review of the literature and report of a case
involving 2% lidocaine. Int J Obstet Anesth 1996; 5:32-5.
[55] Cooper DW, Carpenter M, Mowbray P, et al. Fetal and maternal effects
of phenylephrine and ephedrine during spinal anesthesia for cesarean
delivery. Anesthesiology 2002; 97:1582-90.
[56] Doherty A, Ohashi Y, Downey K, Carvalho JC. Phenylephrine infusion
versus bolus regimens during cesarean delivery under spinal anesthesia:
A double blind randomized clinical trial to assess hemodynamic
changes. Anesth & Analg. 2012; 115:1343-50.
[57] Kunkle K, Ray B, Wolff H. Experimental studies on headache: Analysis
of the headache associated with changes in intracranial pressure. Arch
Neurol Psychiatry 1943; 49:323-58.
[58] Bakshi R, Mechtler LL, Kamran S, et al. MRI findings in lumbar
puncture headache syndrome: Abnormal dural-meningeal and dural
venous sinus enhancement. Clin Imaging 1999; 23:73-76.
[59] Spriggs DA, Burn DJ, French J, Cartlidge NE, Bates D. Is bed rest
useful after diagnostic lumbar puncture? Postgrad Med J 1992; 68:
581-3.
[60] Abouleisu E, Vega S, Blendinger I, Tio TO, Long term follow-up of

epidural blood patch. Anesth Analg 1975; 54:459-63.
[61] Mets B, Broccoli E, Brown, AR. Is spinal anesthesia after failed epidural
anesthesia contraindicated for cesarean section? Anesth ANALG. 1993;
77:629-31.
[62] Pan PH, Bogard TD, Owen MD. Incidence and characteristics of failures
in obstetric neuraxial analgesia and anesthesia: A retrospective analysis
of 19,259 deliveries. Int J Obstet Anesth 2004; 13:227-33.
[63] Ogden CL, Carroll MD, Curtin LR, et al. Prevalence of everweight and
obesity in the United States, 1999-2004. JAMA 2006; 295:1549-55.
[64] Lewis G, Drife J. Why mothers die 2000-2002. Confiedential enquiry
into maternal and child health improving care for mothers, babies and
children.
[65] Hood DD, Dewan DM. Anesthetic and obstetric outcome in morbidly
obese parturients. Anesthesiology 1993; 79:1210-8.
[66] Practice Guidelines for Preoperative Fasting and the Use of
Pharmacological Agents to Reduce the Risk of Pulmonary Aspiration:
Application to Healthy Patients Undergoing Elective Procedures an
updated report by the American Society of Anesthesiologists Committee
on Standards and Practice Parameters. 2010.
[67] Hartsilver EL, Vanner RG. Anesthesia. March 2000; 55(3): 208-11.
[68] Garrad A, Campbell AE, Turley A, Hall JE. Anesthesia. May 2004;
59(5) 435-9.
[69] Jolly M, Sebire N, Harris J, Robinson S. Regan L. The risks associated
with pregnancy in women aged 35 years or older. Human Reproduction.
2000: 15(11):2433-2437.
[70] Pinzaiuti S, Ferrata C, Vanniccini S, Di Rienzo G, et al. Twin
pregnancies after assisted reproductive technologies: The role of
maternal age on pregnancy outcomes. Europ J of Obstet and Gynec. Nov
2016; 206:198-203.
[71] Khalil A, Syngelaki A, Maiz N, Zinevich Y, Nicolaides KH. Maternal
age and adverse pregnancy outcome: A cohort study. Ultrasound Obstet
Gynecol 2013; 634-643.
[72] Sibai BM. Evaluation and management of severe preeclampsia before 34
weeks gestation. Amer J of Obstet and Gynec. Sept 2011; 205(3): 191-
98.
[73] Matthys LA, Coppage KH, Lambers DS, et al. Delayed postpartum
preeclampsia: An experience of 151 cases. Am J Obstet Gynecol. 2004;
190:1464-1466.
[74] Sibai BM, Imitators of severe preeclampsia. Obstet Gynecol. 2007;

109:956-966.
[75] Dyer RA, Pierrcy JL, Reed AR, et al. Hemodynamic changes associated
with spinal anesthesia for cesarean delivery in severe preeclampsia.
[76] Konje JC, Kaufmann P, Bell SC, Taylor DJ. A longitudinal study of
quantitative uterine blood flow with the use of color power angiography
in appropriate for gestational age pregnancies. Am J Obstet Gynecol
2001; 185:608-13.
[77] Silver RM, Landon MB, Rouse DJ, et al. Maternal morbidity associated
with multiple repeat cesarean deliveries. Obstet Gynecol 2006;
107:1226-32.
[78] Oyelses Y, Ananth CV. Placental abruption. Obstet Gynecol. 2006; 108:
1005-16.
[79] Robinson, BK, Grohman WA. Effectiveness of timing strategies for
delivery of individuals with vasa previa. Obstetric Anesthesia Digest.
2012; 32(2): 129-30.
[80] Clark, SL. Amniotic fluid embolism. Obstetrics and Gynecology. 2014;
123(2,Part 1): 337-48.
[81] Jeejeebhoy FM, Zelop CM, Lipman SM, Carvalho BL, et al. Cardiac
arrest in pregnancy: A Scientific Statement from the American Heart
Association. Circulation. 2015; 132(18): 1747-73.
[82] Katz VL, Dotters DJ, Droegemueller W. Perimortem cesarean delivery.
Obstet Gynecol. 1986; 68:571-76.
[83] Katz VL, Balderson K, DeFreest M. Perimortem cesarian delivery: were
our assumptions correct? Am J Obstet Gynecol. 2005; 192:1916-20.
Chapter 6
CHRONIC PAIN MANAGEMENT
Benjamin J. Sloop, MD
Division of Chronic Pain Management
Pain management is a growing subspecialty of anesthesiology that is

playing an ever increasing role in the care of patients. It is a specialty that
many people, physicians included, may not understand. Pain physicians do
much more than prescribe narcotics and are trained to perform interventional
techniques that range from peripheral nerve blocks to rhizotomies to
implantation of devices to manage chronic pain. Understanding the role of the
pain management physician is key to proper utilization, timely referral, and
appropriate therapy.
Pain physicians come from diverse backgrounds to include
anesthesiology, physical medicine and rehabilitation, neurology, internal
medicine, family medicine and psychiatry. A yearlong fellowship is required
and emphasis is placed on treating the patient as a whole, by incorporating
medication management, physical therapy, behavioral therapy, and
interventional techniques. Board certification is provided by several governing
bodies.
Pain has many implications on the patient beyond the physical
ramifications. Many patients also experience social, behavioral, emotional and
financial setbacks as a result of a pain condition. The successful management
90 Benjamin J. Sloop
of these conditions and patients requires more than just medical treatment.
Mental health providers, physical therapists, social services, and physicians
from many backgrounds all play an integral role.
Perhaps pain physicians are best known for their role in the over-
prescription of narcotic medications. This may have been true in the past,
however the future of narcotic prescription for all physicians is rapidly
changing. The Center for Disease Control (CDC) recently published guidelines
on the prescription of narcotic medications and as a result of their guidelines
narcotics will play a much smaller role in the treatment of pain. It is not
unlikely that in the future primary providers and patients alike may require the
expertise of the fellowship trained pain physician to treat pain conditions in the
wake of the scale down of the use of narcotic medications.
The World Health Organization (WHO) pain treatment ladder is an
excellent reference for all providers in an initial effort to prescribe medications
for pain [1]. It suggests starting with non-opioid analgesics such as
acetaminophen and NSAIDs and then escalating to weak opioids and finally to
stronger opioid medications. It also suggests the use of adjuvant medications
which include neuropathic agents, muscle relaxants, anticonvulsants, and
antidepressants. If the physician desires to prescribe narcotics, the recent CDC
guidelines for prescribing opioids for chronic pain should be reviewed [2].
Often, pain medication prescription limitations vary by state and the provider
would be well served by reviewing both the CDC and state guidelines for the
use of narcotics for treating pain.
When receiving narcotic medications from a pain physician, an agreement
or contract is typically signed by the patient. The purpose of this is to protect
the patient from the potential dangers of addictive medications and to ensure
proper use and deter abuse. By signing a contract a patient agrees to random
drug testing and pill counts and to receive pain medication from the office of
the pain physician only. They also agree to not use any illegal substances and
to not divert or share their medications in any way. The violation of any of the
terms of the contract can result in dismissal from the clinic or the
discontinuation of narcotics from the patient’s treatment plan. Should a patient
of a pain physician need narcotic medications in an acute scenario (surgery,
procedure, trauma), the pain physician should be notified by the patient and
the physician providing the service should prescribe a quantity of medication
deemed adequate to control the pain in an average patient.
In many cases, there are interventional therapies that can aid in reducing
pain, whether acute or chronic. The benefit of these therapies is that
medications are delivered directly to the area of pain, thereby having a more
Chronic Pain Management 91
concentrated effect and decreasing the systemic effects of the drug. Examples
of this type of therapy include joint injections and epidural steroid injections.
In some cases these injections are diagnostic as well as therapeutic, confirming
that the nerve or joint injected is in fact the source of the pain. After the area is
confirmed the patient may have surgery to reduce compression of the nerve or
additional interventional therapies to deaden or ablate the nerve. Nerve
ablations usually result in 6 - 12 months of pain relief while the nerve regrows.
Diagnostic blocks are also performed frequently. Examples of diagnostic
blocks include transforaminal epidural steroid injection or single nerve root
injection for radicular pain, facet joint injection or medial branch nerve block
for axial low back pain, geniculate nerve block for knee pain, and third
occipital nerve for cervicogenic headaches.
Contraindications to interventional therapies are few but significant. They
include coagulopathy, current or recent systemic infection, and infection in the
overlying area where the injection would be performed. Patients who are
coagulopathic are at risk for development of a hematoma, the most significant
of which would be in the epidural space following a neuraxial procedure. The
American Society of Regional Anesthesia and Pain Medicine has published
guidelines on the management of anticoagulants for interventional therapies
[3]. The risk of bleeding associated with the procedure determines whether or
not anticoagulation should be held. In some cases, where the risk is not clear,
the guidelines suggest a frank conversation between the pain physician and the
patient regarding the risk and benefits in order to decide whether or not to hold
anticoagulation.
Should a patient be intolerant to or have an aversion to medical therapy
and be unresponsive to or unable to have interventional therapies performed,
neuromodulation or intrathecal drug delivery can be considered. These
therapies should be considered only for chronic pain syndromes as they
involve the implantation of a device that requires invasive surgery and
subsequently involves a screening process as well as a trial. The screening
process involves an evaluation of the patient by a mental health provider to
help determine if the patient is appropriate for an implantable device. This
helps prevent implantation failure and aids in patient selection. There may also
be an insurance requirement prior to implantation. The trial portion of the
process involves a temporary installment of the device to allow the patient to
experience the therapy to determine its efficacy prior to having a permanent
implant placed.
Neuromodulation, also called spinal cord stimulation or dorsal column
stimulation, is the placement of electrical leads in an area corresponding to the
92 Benjamin J. Sloop
pain. Electrical stimulation is applied to the leads and acts to disrupt the pain
signal transmission in accordance with the gate control theory. This technique
currently is limited to the treatment of chronic neuropathic pain. However new
technological advancements are promising and may expand this therapy to
include the treatment of low back pain as would be found in failed back
surgery syndrome. As stated above, the patient who is a candidate for
placement of a spinal cord stimulator would be screened by a mental health
provider and trialed prior to permanent implantation.
Intrathecal drug delivery involves the placement of a catheter in the
intrathecal space through which a continual infusion of medications can be
delivered. The benefits include very little maintenance, much lower doses of
medications used, and few side effects. The limitations include periodic refills
of medications, having an implanted device, and development of tolerance.
This can be performed for a variety of conditions with a variety of medications
infused. For a patient with spasticity, baclofen may be delivered intrathecally.
For a patient with failed back surgery syndrome or cancer pain, opioid
medications or local anesthetics can be infused.
Despite many complicated treatment options and interventional therapies,
there are still areas where the primary care provider and the pain physician can
collaborate in the care of the pain patient. Physical therapy, cognitive
behavioral therapy, chiropractic care, and exercise all have moderate efficacy
for the treatment of chronic back pain and can be prescribed by a primary care
provider [4]. Other ways a primary care physician can impact chronic back
pain include encouraging weight loss and smoking cessation [5].
REFERENCES
[1] World Health Organization. (1996). Cancer pain relief (2nd ed.). Geneva.
[2] Chou, R., Dowell, D., Haegerich, T. CDC Guideline for Prescribing
Opioids for Chronic Pain. MMWR Recomm. Rep. 2016; 65: pages 1-49.
[3] Narouze, S., Benzon, H. T., Provenzano, D. A., Buvanendran, A., De
Andres, J., Deer, T. R., Huntoon, M. A. Interventional Spine and Pain
Procedures in Patients on Antiplatelet and Anticoagulant Medications.
Regional Anesthesia and Pain Medicine. 2015; 40 (3): 182-202.
[4] Chou, Roger, Huffman, Laurie Hoyt. Nonpharmacologic Therapies for
Acute and Chronic Low Back Pain: A Review of the Evidence for an
American Pain Society/American College of Physicians Clinical
Practice Guideline. Ann. Intern. Med. 2007; 147 (70): 492-504.
Chronic Pain Management 93
[5] Andersen R. E., Crespo C. J., Bartlett S. J., Bathon J. M., Fontaine K. R.
Relationship between body weight gain and significant knee, hip, and
back pain in older Americans. Obes. Res. 2003; 11(10): 1159–1162.
Chapter 7
ANESTHESIOLOGIST INTENSIVISTS:
CRITICAL CARE ANESTHESIOLOGY
Habib Srour, MD
Society at large has been enveloped in the impact of improvements in

healthcare. In each specialty - where once there was a paucity of options for
many ailments - there are now numerous avenues that involve significant
training, sub-specialization, and resources. As medicine has advanced, the
need for critical care specialists has grown. It has expanded in such a way that
physicians with multiple backgrounds can arrive at a formal education in
critical care medicine. Anesthesiology and perioperative medicine provide one
such avenue that is uniquely suited and long proven in the history of medicine.
The first respiratory care units in the 1950s were established and staffed
by anesthesiologists. This framework led to the modern model in much of
Europe where anesthesiologists receive training in critical care as part of their
residency program. Many intensive care units are staffed by anesthesiologists
in those regions. Critical care in the United States has followed a different path
and has a varied and disparate set of circumstances for staffing of these units
depending upon multiple factors. There are intensivists that are internal
medicine physicians who train in pulmonary medicine and critical care and
frequently staff medical units. Rheumatologists, nephrologists, and infectious
disease specialists are among many specialties that can train in critical care
96 Habib Srour
from an internal medicine background. Surgeons, emergency physicians,

neurologists, and anesthesiologists help comprise the list of specialists that
pursue critical care medicine training in the absence of an internal medicine
background.
Anesthesiologists have a well-established role in the history of critical
care. As a specialty frequently confronted with patients in extremis, it has
played a pivotal role in the development of monitoring, resuscitation
interventions, and patient safety. The American Board of Anesthesiology was
the first specialty board to offer a special qualification examination process in
critical care medicine. Many recognizable figures that contributed to the
modern understanding of critical illness and treatment were anesthesiologists
including Severinghaus, Pontoppidan, Bendixen, Downs, Kirby, and Safar,
among others. Indeed, the president of the Society of Critical Care Medicine at
the time of this writing is an anesthesiologist.
Training in anesthesiology and perioperative medicine involves a focus on
respiratory management, treatment of shock states, sedation, analgesia,
delirium, blood glucose management, and transfusion medicine. These are
significant issues that present commonly in the operating room and in the
critical care arena. Formal training in airway management, ventilator
management, pain management, invasive monitoring, surgical management,
massive transfusion, hemorrhage, patient safety, and point-of-care testing such
as ultrasound are all part and parcel to anesthesiology and, indeed, critical
care.
In the same way that an internist is a logical choice to manage chronic and
pervasive health derangements, anesthesiologists are - by the nature of daily
interactions with acute and hyperacute situations - a logical choice for acute
critical care management. This is particularly true in the post-operative patient.
Daily exposure and management of mechanical ventilation in the operating
room gives insight for the decisions to be made regarding continued invasive
ventilation and, indeed, the cessation of it. Anesthesiologists manage every
imaginable airway situation due to the daily intentional induction of an
otherwise dangerous situation; this is safely accomplished due to the
applicable skills necessary to prevent catastrophe. Outside of general
anesthesia for procedures, anesthesiologists provide sedation and pain control
for a plethora of awake patients through a variety of invasive undertakings.
This imparts an intimate familiarity with pain, its control, and its implications
– all of which are considerations in the critically ill. The hemodynamic
implications of many operations are second-nature to the trained
anesthesiologist and this serves well in the acute post-operative period.
Anesthesiologist Intensivists 97
Management of massive hemorrhage, tourniquet use, liver reperfusion, left-

heart bypass, and aortic cross-clamping are some examples of the innate
physiologic drama that must be addressed by the anesthesiologist.
Obtaining board certification in anesthesiology requires four years of post-
graduate education in the United States. The addition of a critical care
fellowship adds one year of training. Colleagues in the medical specialties
undergo three years of medicine residency followed by one year of critical
care fellowship in concert with two years of an associated subspecialty –
typically pulmonary medicine. The high rate of burnout in critical care due to
its taxing nature is often mitigated by dividing time between the high-acuity
unit and some other arena. In the case of anesthesiologists, this often means
the operating room or the pre-operative clinic. The derangements in
physiology that result from an operation allow anesthesiologists to be uniquely
suited to surgical critical illness. The diagnoses involved are frequently
indications for operations and/or the direct result of the pathology that led to
an operation.
The study of perioperative medicine allows a hybrid focus on medical and
surgical physiology. Given that critical care costs have been estimated to be
roughly 1% of the American GDP, anesthesiologist intensivists providing care
for perioperative critical illness can minimize such ballooning costs by
improving outcomes. Patients undergoing neurologic surgery or interventional
procedures for stroke with their associated unique hemodynamic implications
and monitoring are managed intraoperatively and in the intensive care unit by
anesthesiologists. Cardiac and thoracic surgical patients with their ventilator
support challenges, trans-esophageal echocardiography use, cardiopulmonary
bypass exposure, extra-corporeal membrane oxygenation, and ventricular
assist devices are also managed by anesthesiologists in both the operating
rooms and the intensive care units. Head and neck surgeries by
otolaryngologists and oral-maxillofacial surgeons have implications for airway
access and recovery for which anesthesiologists are distinctively trained.
The American Society of Anesthesiology is advancing the concept of the
perioperative surgical home (PSH) whereby customer service, accountability
for quality of care, continuity of care, and co-management with surgeons are
explicit tenets. This naturally follows in the critically ill subset of patients and
their providers. In the PSH model, the anesthesiologist provides medical
assessment, diagnosis, respiratory and cardiovascular support, and infection
control. Anesthesiologists are equipped with the knowledge and technical
expertise to address a wide variety of emergency and trauma situations. Along
with colleagues in other areas of critical care medicine, anesthesiologists help
98 Habib Srour
provide an essential service to patients around the world both during their
surgery and during their recovery.
REFERENCES
ASA Public Education Series.
Kash B, Cline K, Menser T, Zhang Y. The Perioperative Surgical Home
(PSH) - A Comprehensive Literature Review for the American Society of
Anesthesiologists. June 12, 2014. https://www.asahq.org/psh/resources/
an%20overview.
Chapter 8
NPO GUIDELINES
Brooke A. Bauer, MD
“When did you last have anything to eat or drink?” The perioperative
care team emphasize the importance of patient fasting prior to any
elective procedure, yet so few truly understand why the answer is
important.
As early as 1946 it was noted that the laryngeal muscles relax during
general anesthesia and can lead to aspiration events. Mendelson described the
effects of aspiration on the respiratory system in a parturient as a picture of
obstruction or bronchospasm leading to pulmonary edema and severe lung
injury with possible death. He published his findings during this time period to
emphasize to his colleagues the importance of emptying the stomach prior to
general anesthesia.1
Through the years many different techniques were used to decrease the
risk of aspiration events during anesthesia. Patient fasting was the most
common approach to reduce this risk. However, a general consensus for
recommendations on “Nil per os” (NPO) time did not exist until several
decades later. Even though aspiration is a rare event with an approximate
incidence of 6.5/10,000 anesthetics, serious consequences of morbidity and
100 Brooke A. Bauer
mortality made recommendations a long awaited resource for anesthesia

providers.2,3 In 1999, the American Society of Anesthesiologists (ASA)
published the “Guidelines for Preoperative Fasting and the Use of
Pharmacologic Agents to Reduce the Risk of Pulmonary Aspiration:
Application to Healthy Patients Undergoing Elective Procedures.” These
recommendations were based on articles published between 1940 and 1996. In
2011 the ASA updated the Guidelines to include 158 research articles
published from 1996-2010. Similar to Mendelson’s objective, the purpose of
the original guidelines was to: “
 Enhance the quality and efficiency of anesthesia care

 Stimulate evaluation of clinical practices
 Reduce the severity of complications”4
A Task Force of ten members, anesthesiologists and a consulting

methodologist, composed the Guidelines. To provide the strongest level of
evidence for development of the Guidelines, this team reviewed published
articles relating to aspiration risk during the perioperative period, consulted
experts in the field, and conducted open forums at national meetings for input
from a large community of anesthesiologists. Even though numerous studies
were reviewed during construction of these guidelines, it is difficult to obtain
specific information about such a rare event. In lieu of direct observational
studies of aspiration events, factors thought to increase the severity of
symptoms post-aspiration were used as surrogates, such as residual gastric
volume and gastric pH measurements.4
Before going into detail about the information included in the ASA
Fasting Guidelines, one important element to keep in mind is the definition of
a “standard” versus a “guideline.” According to the U.S. National Library of
Medicine, “Standards are authoritative statements that articulate minimal...
levels of performance…. Guidelines are statements of principles or procedures
that assist professionals in ensuring quality.”5 Therefore, anesthesia providers
use the ASA Fasting Guidelines as framework for determining a safe fasting
interval for the patient. There is still much research to be done in this area, so
even though guidelines are in place, a vast amount of ambiguity still exists and
will be obvious throughout this chapter.
The recommendations were constructed for application to healthy patients
who are having an elective surgery or procedure where an anesthesia provider
will administer general anesthesia, regional anesthesia or sedation.4 Since
there is evidence to suggest that patients who have comorbidities are at
NPO Guidelines 101
increased risk for aspiration events, clinicians may choose to adjust the
recommended fasting time for patients with more complex medical histories.6
It is common practice for anesthesiologists to be more conservative when
deciding a safe NPO time, especially if the patient’s comorbidities could
contribute to delayed gastric emptying. However, the healthy patient is a good
starting point for understanding the recommendations.
There are four main categories of food or drink intake to consider when
determining the amount of time that should pass prior to undergoing
anesthesia. These categories include clear liquids, breast milk, infant formula,
and solids/non-human milk.
CLEAR LIQUIDS
A “clear liquid” incorporates more than the name implies. A general rule
for inclusion in the “clear liquid” category is, if you can see through it, it
probably belongs here. Examples include water, juice without pulp, sodas,
sport drinks and black coffee, i.e., liquids that are non-particulate or contain no
fat.
The Guidelines recommend that a patient fast for at least 2 hours
following ingestion of a clear liquid prior to undergoing anesthesia. The
supporting evidence is derived from a meta-analysis of randomized controlled
trials that compared gastric volumes in patients who had consumed clear
liquids 2-4 hours and more than 4 hours prior to measurement. The adults who
consumed clear liquids 2-4 hours prior to measurement, surprisingly, had
smaller gastric volumes. Researchers also conducted studies comparing the pH
of the stomach contents for these groups of patients and showed that patients
who ingested clear liquids 2-4 hours prior had a higher gastric pH.7-14 With the
vast amount of evidence supporting this recommendation, the experts easily
came to a consensus that one should wait for at least 2 hours following
consumption of a clear beverage prior to undergoing anesthesia.4
BREAST MILK
According to the Guidelines, a child should not be given breast milk
within 4 hours of a scheduled procedure for which he/she will need anesthesia.
The studies behind this recommendation are observational and report
102 Brooke A. Bauer
inconsistencies with gastric volume and pH level measurements. The articles

cited by the ASA Guidelines conclude that breast milk is not safe to give to an
infant at 2 and 3 hours prior to anesthesia and that infants who fast for 3-4
hours do not routinely become hypoglycemic intraoperatively.15-17 The Task
Force recommended fasting 4 hours after intake of breast milk to balance the
risk of aspiration with the risk of developing hypoglycemia.4
INFANT FORMULA
The recommendations for fasting when considering ingestion of infant
formula are to wait at least 6 hours from last consumption prior to anesthesia.
These recommendations are again based on a study that found little difference
in gastric fluid volume when comparing infants who fasted for 4 versus 8
hours after having formula.18 Formula is thought to be more complex and
require longer for the breakdown than breast milk, which aids in the digestion
of its own fat content.19 This reasoning appears to support the 2 hour
difference in the recommendations between human milk and formula fasting
times.4
SOLIDS/NON-HUMAN MILK
Multiple studies were used to make the recommendations for this
category. First, a randomized controlled trial was performed in 1983,
comparing the residual gastric contents and gastric pH of patients who had
consumed a light meal 4 hours prior to anesthesia and those who had fasted
overnight.20 A “light meal” consisted of one slice of buttered toast and a cup of
tea or coffee with milk. This study showed no difference between the residual
gastric volume or pH of these two groups of patients.20 A second, non-
randomized study compared children who had fasted for more than 4 hours
with those who had consumed biscuits/non-human milk 4 hours or less prior to
a procedure. In contrast to the last findings, these results showed higher gastric
volumes in the non-fasting children but no difference in the gastric pH.21 An
observational study then suggested that children who fast for more than 8
hours may develop hypoglycemia.22 From this information the Task Force
concluded that one should fast for 6 hours following a light meal/non-human
milk and 8 hours following a fatty meal prior to having anesthesia.4
NPO Guidelines 103
Recommendations for minimum number of fasting hours
Clear Liquids 2
Breast-milk 4
Formula 6
Non-human milk/Light meal 6
Heavy/Fatty meal 8
The recommendations above are based on the ASA Guidelines, yet these
are not dramatically different from the European Society of Anaesthesiology
(ESA) guidelines for perioperative fasting. The ESA guidelines have two
categories: clears (2 hours) and solids (6 hours). One key difference between
the ASA and ESA Guidelines include the ESA’s emphasis on continuing to
drink clear liquids up to 2 hours prior to surgery to help decrease anxiety and
adverse effects of prolonged fasting. Another dissimilarity is that European
anesthesiologists will accept a small amount of milk in tea or coffee as a clear
liquid, while most American anesthesiologists would categorize this as “non-
human milk.” In contrast to the ASA’s ambiguity with many topics, the ESA
guidelines specifically suggest to abstain from canceling a case due to chewing
gum, hard candy, or smoking. Along these same lines, the ESA recommends,
“Patients with obesity, gastro-oesophageal reflux and diabetes and pregnant
women not in labour can safely follow all of the above guidelines.”23
The American guidelines do err on the side of caution and leave room for
interpretation, which could be due to the high rate of litigation for medical
adverse events in the United States.24 Since there are no clear
recommendations in the ASA Guidelines concerning hard candy, chewing
gum or smokeless tobacco, in the United States it becomes the responsibility
of the individual clinician to determine a safe fasting time for the patient.
Some investigators have looked into these matters, providing guidance for the
clinician. For example, in a prospective randomized study, chewing gum given
to patients just prior to a procedure did not significantly affect gastric volume
or pH compared to patients who did not chew gum.25 However, strong
evidence is not available to make recommendations for every scenario.
Another questionable topic is that of smoking. Most American
anesthesiologists would agree with the ESA on this standpoint and not cancel
or delay a case due to a patient having recently smoked tobacco.
Even though the literature may not provide specific information to define
a patient’s risk of aspiration and the amount of risk providers can control by
enforcing fasting times, it seems that anesthesiologists across the world mostly
104 Brooke A. Bauer
agree with and follow the preoperative fasting guidelines recommended by the
ASA. The current research in this area is moving in a new direction through
assessment of gastric volume and content through ultrasound imaging.26,27 A
point-of-care ultrasound trained anesthesia provider may be able to assess
gastric volume prior to anesthesia induction to identify patients at risk for
aspiration during anesthesia induction independent from NPO status. Once the
studies using this technique gain in frequency and acceptance, ultrasound
imaging of the gastric contents may become the future surrogate for assessing
aspiration risk and could contribute material for Guideline revision.
Again, the ASA Fasting Guidelines were formulated for application to
healthy patients undergoing elective procedures. The final determination of the
appropriate fasting time is up to the discretion of the anesthesia provider. With
the above statement in mind, it may not be appropriate to tell all patients to
abstain from eating and drinking after midnight prior to a procedure. However,
with the high frequency of schedule adjustments, it may not be possible to
guarantee that coffee and toast at 0600 is a good idea for a scheduled 1200
procedure because it may change to 1000 without notice. Thus, early
communication among the patient, surgeon/proceduralist, nursing care, and
anesthesiologist could be beneficial to ensure safe and efficient care for a
patient.
In essence, the anesthesia provider and medical care teams should keep
these fasting Guidelines in mind when caring for a patient who is to undergo
anesthesia. Ultimately, the anesthesiologist should use his or her clinical
judgement for each individual to determine a safe plan of care.
REFERENCES
[1] Mendelson CL. The aspiration of stomach contents into the lungs during
obstetric anesthesia. Am J Obstet Gynecol 1946;52:191-205.
[2] Cohen MM, Duncan PG, Pope WDP, Wolkenstein C. A survey of
112,000 anesthetics at one teaching hospital (1975-83). Can Anaesth Soc
J 1986; 33:22-31.
[3] Olsson GL, Hallen B, Hambraeus-Jonzon K. Aspiration during
anaesthesia: a computer-aided study of 185,358 anaesthetics. Acta
Anaesthesiol Scand 1986; 30:84-92.
[4] ASA Committee on Standards and Practice Parameters, et al. Practice
Guidelines for Preoperative Fasting and the Use of Pharmacologic
Agents to Reduce the Risk of Pulmonary Aspiration: Application to
Healthy Patients Undergoing Elective Procedures. An Updated Report
NPO Guidelines 105
by the American Society of Anesthesiologists Committee on Standards

and Practice Parameters. Anesthesiology 2011; 114(3):495-511.
[5] National Institutes of Health. Collection Development Manual:
Standards and Guidelines. U.S. National Library of Medicine. <
https://www.nlm.nih.gov/tsd/acquisitions/cdm/formats46.html>
Accessed 12/24/2016.
[6] Warner MA, Warner ME, Weber JG. Clinical significance of pulmonary
aspiration during the peri-operative period. Anesthesiology 1993;78:56-
62.
[7] Agarwal A, Chari P, Singh H. Fluid deprivation before operation. The
effect of a small drink. Anaesthesia 1989; 44:632-4.
[8] Hutchinson A, Maltby JR, Reid CR. Gastric fluid volume and pH in
elective inpatients. Part I: Coffee or orange juice versus overnight fast.
Can J Anaesth 1988; 35:12-5.
[9] Maltby JR, Sutherland AD, Sale JP, Shaffer EA. Preoperative oral
fluids: is a five-hour fast justified prior to elective surgery: Anesth Analg
1986; 65:1112-6.
[10] McGrady EM, Macdonald AG. Effect of the preoperative administration
of water on gastric volume and pH. Br J Anaesth 1988; 60:803–5
[11] Phillips S, Hutchinson S, Davidson T. Preoperative drinking does not
affect gastric contents. Br J Anaesth 1993; 70:6 –9
[12] Read MS, Vaughan RS. Allowing pre-operative patients to drink:
Effects on patients’ safety and comfort of unlimited oral water until 2
hours before anaesthesia. Acta Anaesth Scand 1991; 35:591–5
[13] Sutherland AD, Maltby JR, Sale JP, Reid CR. The effect of preoperative
oral fluid and ranitidine on gastric fluid volume and pH. Can J Anaesth
1987; 34:117–21
[14] Yagci G, Can MF, Ozturk E, Dag B, Ozgurtas T, Cosar A, Tufan T.
Effects of preoperative carbohydrate loading on glucose metabolism and
gastric contents in patients undergoing moderate surgery: A randomized,
controlled trial. Nutrition 2008; 24:212– 6
[15] Litman RA, Wu CL, Quinlivan JK. Gastric volume and pH in infants fed
clear liquids and breast milk prior to surgery. Anesth Analg 1994;
79:482-5.
[16] Sethi AK, Chatterji C, Bhargava SK, Narang P, Tyagi A. Safe pre-
operative fasting times after milk or clear fluid in children. A
preliminary study using real-time ultrasound. Anesthesia 1999 Jan;
54(1):51-9.
[17] Van der Walt JH, Foate JA, Murrell D, Jacob R, Bentley M. A study of
preoperative fasting in infants aged less than three months. Anesth
Intensive Care 1990; 18:527-31.
[18] Cook-Sather SD, Harris KA, Chiavacci R, Gallagher PR, Schreiner MS.
A liberalized fasting guideline for formula-fed infants does not increase
106 Brooke A. Bauer
average gastric fluid volume before elective surgery. Anesth Analg

2003; 96:965-9.
[19] Jensen RG, Hagerty MM, McMahon KE. Lipids of human milk and
infant formulas: a review. Am J Clin Nutr 1978 Jun; 31(6):990-1016.
[20] Miller M, Wishart HY, Nimmo WS. Gastric contents at induction of
anaesthesia: Is a 4-hour fast necessary? Br. J. Anaesthes. 1983; 55:
1185-88.
[21] Meakin G, Dingwall AE, Addison GM. Effects of fasting and oral
premedication on the pH and volume of gastric aspirate in children. Br J
Anaesth 1987; 59:678-82.
[22] Thomas DK. Hypoglycaemia in children before operation: Its incidence
and prevention. Br J Anaesth 1974; 46:66-8.
[23] Smith I, Kranke P, Murat I, Smith A, O’Sullivan G, Soreide E, Spies C,
Veld BI. Perioperative fasting in adults and children: guidelines from the
European Society of Anaesthesiology. Eur J Anaesthesiol 2011; 28:556-
569.
[24] Jena AB, Seabury S, Lakdawalla D, Chandra A. Malpractice risk
according to physician specialty. N Engl J Med. 2011; Aug 18;
365(7):629-636.
[25] Goudra BG, Singh PM, Carlin A, Manjunath AK, Reihmer J, Gouda
GB, Ginsberg GG. Effect of gum chewing on the volume and pH of
gastric contents: A prospective randomized study. Digestive Diseases
and Sciences. April 2015; 60(4):979-983.
[26] Perlas A, Mitsakakis N, Liu L, Cino M, Haldipur N, Davis L, Cubillos J,
Chan V. Validation of a mathematical model for ultrasound assessment
of gastric volume by gastroscopic examination. Anesthesia-Analgesia.
Feb 2013; 116(2):357-363.
[27] Perlas A, Chan V, Lupu C, Mitsakakis N, Hanbidge A. Ultrasound
assessment of gastric content and volume. Anesthesiology. 2009;
111:82-9.
Chapter 9
THE HISTORY OF NURSE ANESTHESIA
Charles Jonathan Fletcher, APRN, CRNA, BSN, MSN

INTRODUCTION
The profession of nurse anesthesia evolved out of a need for patient safety
after physicians began performing surgical procedures using anesthetic agents.
For over 150 years, nurse anesthetists have been administering anesthesia
during surgical procedures. In the United States there are more than 49,000
Certified Registered Nurse Anesthetists (CRNAs) and student registered nurse
anesthetists who provide approximately 40 million anesthetics a year.
The advent of anesthetic agents provided surgeons with conditions where
patients were no longer being held down to perform procedures. These agents
allowed surgical conditions that blunted the patient’s response to pain and
allowed the surgeon to concentrate on the procedure. Chloroform, ether and
nitrous oxide provided analgesia and amnesia of the surgical experience. Early
in the history of administrating anesthesia, the most junior surgical staff
member, medical student or even a layperson such as a hospital porter, family
member, or friend was briefly instructed on how to administer the anesthetic
gas. Complications from anesthesia were common and often deadly. Nurses
filled these voids and provided expert care as anesthetists.
108 Charles Jonathan Fletcher
The first reported examples of nurses providing anesthesia date to the

Civil War. While “… army doctors and nurses had experience with using ether
by the time of the Civil War, chloroform became popular during the
conflict...” Nurse anesthesia pioneers like Catherine Lawrence and others
provided anesthesia during the Civil War. Lawrence wrote in her 1896
autobiography, “The worse cases of the wounded the doctor attended to. I also
tied arteries and administered chloroform.”
In 1863, Mrs. John Harris, a nurse from Philadelphia, was at the front all
during the war delivering anesthesia to Civil War soldiers. On July 3rd, she
received government approval to take supplies to Gettysburg. Her personal
mission is described in the following quote. “Taking some chloroform and
stimulates, she left Baltimore on the 4th, and penetrated as near as possible to
the scene of the conflict, ministering as much as in her power to the stream of
the wounded …”
At the beginning of the fourth quarter of the 19th century, nurse anesthesia
made the leap into healthcare as a profession when Sister Mary Bernard
became the first individual to be recognized as a nurse anesthetist. In 1877 she
entered St. Vincent’s Hospital in Erie Pennsylvania to begin a nursing career
and then transitioned to serve as a nurse anesthetist. The professional transition
continued as other nurses began to function in the role as anesthetist. In 1880
Sister Aldonza Eltrich was trained as an anesthetist at the newly built St.
John’s Hospital in Springfield, Illinois. The expansion of the role of the nurse
anesthetist continued in the Catholic Church run hospital, as seen in the quote
from Thatcher, a nurse anesthetist and author. “…records, fragmentary as they
are, not only give a glimpse of what was undoubtedly a prevailing practice in
many Catholic hospitals but also show the beginning of a trend.”
In 1889 in Rochester, Minnesota, St. Mary’s Hospital opened in a joint
venture between the church and the Mayo brothers. Edith Graham was initially
hired as head of nursing staff, however, she and her sister Dinah-also a nurse,
quickly transitioned to providing anesthesia. While Dinah would only work as
an anesthetist for a short period, Edith continued to work until later marrying
Charles Mayo. In 1893, Alice Magaw began her career as an anesthetist for the
Mayo surgeons. She reported to have completed 1,092 cases of anesthesia
“without an accident, the need for artificial respiration, or the occurrence of
pneumonia or any serious results.” She is described as the “mother of
anesthesia” for her expertise of open drop ether.
The next progression was the establishment of nurse anesthesia training.
During the end of the 19th and the beginning of the 20th century, learning the
art of providing anesthesia meant traveling to a well-known medical center for
The History of Nurse Anesthesia 109
training. The Mayo brothers’ use of nurse anesthetists began to spread through
the medical community across the country. Medical literature began to make
note of the role of the nurse anesthetist as well. Many surgeons, after
observing procedures at the Rochester facility, sent nurses to train under the
tutelage of the Mayo nurse anesthetists, Alice Magaw and Florence
Henderson, for periods of 2 to 3 months. In 1909, following a physician intern
revolt against providing anesthesia, Agnes McGee opened the first school of
nurse anesthesia at St Vincent’s Hospitals in Portland Oregon. The hospital’s
loss of the use of interns to deliver anesthesia provided an opportunity for the
school to be established and it “expanded and flourished under McGee’s
leadership.”
Schools of anesthesia began to organize around the country. The School of
Nursing at St John’s Hospital in Springfield Illinois was restructured in 1912.
A postgraduate training program was offered with a course in anesthesia and
in 1924 secular nurses were granted admission for postgraduate training. After
developing a course in anesthesia in 1912, the New York Post-Graduate
Hospital School opened their School of Anesthesia. The six-month course had
four nurse “etherizers” and four ether students in residence.
Prior to the United States joining the fight in World War I, American
nurses began providing anesthesia in the conflict in 1914 with service as
members of military related medical organizations. With the United States’
entry into the conflict in 1917, the military began to use nurse anesthetists for
wartime service. As the US role escalated, the military’s need for expert
anesthetists increased. This lead to an arrangement for student anesthetists in
the Army Nurse Corps to be sent to the Mayo clinic to be trained as
anesthetists. The Navy developed a mirror program to the Army’s program
with the student anesthetist from the Navy attending a three-month program at
the Pennsylvania Hospital in Philadelphia. These medical facilities provided
training for US and British nurses through a program developed by the Red
Cross and directed by the General Medical Board of the Council for National
Defense.
In 1915, the formal founding of the influential Lakeside Hospital School
of Anesthesia occurred in Cleveland, Ohio. Surgeon George Crile and nurse
anesthetist Agatha Hodgins, both widely known for their expertise in
anesthesia, developed an education curriculum that was the foundation of
anesthesia training that 54 other institutions used as a program template for
their own six-month-long postgraduate anesthesia training. The school trained
nurses, physicians and dentists in the science of anesthesia. The program was
briefly closed in 1917 when the Ohio Medical Board questioned the legality of
nurses providing anesthesia in the court system. However the legal precedent
for nurses providing anesthesia was established and the school reopened its
doors in 1918 and graduated 54 nurses and 2 physicians by the end of 1919.
The legality of nurse anesthesia practice was further defined when anesthesia
practice was challenged in court in the state to the south of the Ohio border. In
the case Frank v. South, the 1917 Kentucky court ruling established that “…a
nurse giving anesthesia was not engaged in the practice of medicine…” and is
an example of healthcare practice that is included in the field of nursing and
medicine. This ruling set the precedence for nurse anesthesia as a nursing
specialty. From 1915 to 1920, approximately ten anesthesia schools populated
the anesthesia educational system.
Another pioneer in the nurse anesthesia field was Alice Hunt. In 1908, she
began her training in open drop ether and nitrous oxide/ether anesthesia
administration. In 1917 she was asked to replace a nurse anesthetist at Peter
Bent Brigham Hospital in Boston who had been the deployed overseas for the
war. Hunt developed a reputation as a skilled anesthetist with the use of
nitrous oxide and oxygen while also training both nurses and medical interns
in the art of anesthesia. Later in 1920 she was published in the Archives of
Surgery with an article she co-authored with a surgeon discussing
postoperative complications. At the end of World War 1, Yale asked Hunt to
join their staff as an anesthetist. In 1922, she received a university appointment
as instructor of anesthesia and then in 1930, she received a promotion to
assistant professor. She would spend 26 years teaching nurses and medical
students’ anesthesia. Her book Anesthesia: Principles and Practice, was the
first textbook of anesthesia authored by a nurse anesthetist.
In 1931 the first national nurse anesthesia organization, the National
Association of Nurse Anesthetists (NANA), was founded by Agatha Hodgins.
The association was the foundation for what would later become the American
Association of Nurse Anesthetist (AANA) in 1939.
In the 1940s, as the United States moved into World War II, the Army
Nurse Corps developed a six-month nurse anesthesia course to fill the shortage
of anesthesia providers in the war theater. This program trained more than
2000 nurse anesthetists. Nurse anesthetists outnumbered anesthesiologists by a
ratio of 17 to 1 in 1942. In 1944 AANA membership was granted to female
African-American nurse anesthetists and then in 1947 membership was then
granted to male nurse anesthetists. That same year the first issue of the AANA
News Bulletin was published.
As the 1950s began, AANA membership passed 5,000 members. In 1951,
during the Korean War, the United States Air Force (USAF) began
development of the first nurse anesthesia training program under the Air Force
Program Training Requirement HQ USAF directive. In 1952 schools were
opened at Sampson Air Force Base in Geneva, New York and Lackland Air
Force Base in San Antonio, Texas. In this year in January, the AANA
undertook its accrediting process for nurse anesthesia school. The Bolton Act
eliminated the restriction against male nurses in the military
In 1971, Mount Marty College in Yankton, South Dakota accepted the
first Bachelors degree students into their anesthesia program. This was the first
program to offer a Bachelors degree in nurse anesthesia. The following year,
AANA membership passed 15,000. John Garde, CRNA, in 1972, was elected
as president of the AANA, making him the first male president of the
Association. Then in 1973, Goldie Brangman, CRNA was elected as president
of the AANA and was the first African American president of the association.
In 1974 the AANA established “Standards for Nurse Anesthesia Practice.” In
1975, the American Society of Anesthesiology challenged the right of the
AANA to accredit nurse anesthesia programs. Their challenge was
unsuccessful. In 1978, the Kaiser Permanente Nurse Anesthesia Program
graduated their first students with a master’s of science degree. This program
was the first to grant a master’s degree in nurse anesthesia.
The 1980’s began a change in reimbursement of CRNA services. The Tax
Equity and Fiscal Responsibility Act of 1982 (TEFRA) laid out medical
direction requirements for anesthesiologist to receive reimbursement for cases
performed by a qualified anesthetist. While “Anesthesiologist medical
direction of CRNA services is not required by the Medicare program; rather,
medical direction is defined by Medicare Part B…” Later in 1984, the Deficit
Reduction Act of 1984 provided a measure, a three year pass-through
provision, that assured hospitals using CRNAs that “they would not lose
money by employing CRNAs.” The AANA would later lobby for and help
establish legislation that would secure “direct reimbursement of CRNA
services through Medicare Part B.” In 1986, CRNAs received direct
reimbursement rights under Medicare regulations. This landmark legislation,
which went into effect in 1989, provided the first Medicare reimbursement to a
nursing specialty and or non-physician group.
In January 2000, in the waning days of the Clinton (whose mother was a
nurse anesthetist) administration, a rule change in CRNA supervision was
published. “Under that rule, State laws would control which professionals
would be permitted to administer anesthesia and the level of supervision
required for CRNAs.” This new rule would be short lived. The Bush
administration would delay implementation by enacting multiple review
periods. On November 13, 2001, a new rule was published which states, “This
final rule maintains current physician supervision requirements for certified
registered nurse anesthetists (CRNAs), unless the Governor of a State, in
consultation with the State’s Boards of Medicine and Nursing, exercises the
option of exemption for this requirement consistent with State law.” While the
new rule maintained the supervision requirement for Medicare, it provided
state Governors with the ability to “Opt Out” of the Medicare physician
supervision for CRNAs in their state. In December 2001, Iowa became the
first state to exercise the opt out clause for federal physician supervision of
CRNAs. 17 states later chose to enact this provision. In 2002 membership in
the AANA surpassed 30,000 members.
In the summer of 2004, Victor Ortiz, CRNA, challenged a Florida Board
of Medicine ruling from 2002 which required an anesthesiologist to supervise
CRNA practice in the office based surgery cases. Previously, a physician
supervised CRNA practice in this setting. On July 21, 2004, the Forth District
Court of Appeal ruled in favor of Ortiz reversing a previous decision. “The
court noted that under the Nurse Practice Act, a CRNA may be supervised by
any licensed physician. The court also concluded that if the Board of Medicine
cannot restrict the practice of CRNAs indirectly through the discipline of
physicians then it cannot restrict CRNAs directly.” This ruling allowed
CRNAs to return to the Florida office based surgery practices they were forced
to leave in 2002.
The AANA on June 17, 2006 celebrated its 75th anniversary. The AANA
Annual Meeting featured former President Clinton as the keynote speaker. The
former President’s mother and grandmother were nurse anesthetists.
In 2007, the Council on Recertification of Nurse Anesthetists (COR) and
the Council on Certification of Nurse Anesthetists (CCNA) created a separate
and independent National Board of Certification and Recertification for Nurse
Anesthetists (NBCRNA). The NBCRNA becomes the driving force behind a
recertification exam movement.
In 2007, in a State of Montana Supreme Court opinion, it was affirmed,
“Montana state law does not require nurse anesthetists to be supervised by
physicians.” Their opinion confirms the 2004 gubernatorial Montana opt out
of Medicare and Medicaid supervision requirements.
In 2008, AANA membership passed 40,000 members. On December 11,
2008, the Centers for Medicare and Medicaid Services (CMS) issued new
practice guidelines for Medicare hospital conditions for anesthesia services.
Through the advocacy of the AANA, the following guidelines were adopted:
1) Medicare no longer required physician supervision of labor and

delivery analgesia and moderate sedation services provided by
CRNAs.
2) Medicare required that deep sedation with propofol in the operative
setting must involve an anesthesia professional such as a CRNA
3) Individual operating practitioners did not need to be granted privileges
to supervise a CRNA.
In 2009, the AANA legal council “filed an amicus (“friend of the court”)
brief in the Louisiana pain management case.” Their intent was to bring the
brief before the Supreme Court of Louisiana. The court denied the hearing and
“Louisiana continued to be the only state in the nation to rule that
interventional pain management is not within the CRNA scope of practice.”
In the August 2010 issue of Health Affairs, the article titled “No Harm
Found When Nurse Anesthetists Work Without Supervision By Physician”
was published. The article examined data from Medicare for the time between
1999 and 2005. This analysis found “… no evidence that opting out of the
(physician) oversight requirement resulted in increased inpatient deaths or
complications.” The article went on to state, “These results do not support the
hypothesis that allowing states to opt out of the supervision requirement
resulted in increased surgical risks to patients.”
In 2016 the long discussed NBCRNA recertification requirements begin.
The recertification requirements will include tested CEUs, standard CEUs, and
a recertification exam. The first exam, a practice exam, will be required by the
end of the 2024 or 2025 recertification periods and then a qualifying
recertification exam will be required at the end of the next eight year cycle in
2032 or 2033. Passing of the second recertification exam will be required to
continue practicing as a CRNA.
The role of the CRNA in the United States provides millions of patients
access to health care each year. As stated in the opening paragraph, CRNAs
provide approximately 40 million anesthetics each year in all 50 states plus the
District of Columbia. The CRNA is educated in a Masters or Doctorate Nurse
Anesthesia program that is accredited by the Council of Accreditation of
Nurse Anesthesia Educational Programs. Students who are accepted after
January 1, 2022 into accredited nurse anesthesia programs will graduate with
doctoral degrees. While student acceptance is individually managed by each
schools admissions department, most programs require a BSN, a current
nursing license, one year of recent critical care nursing experience such as
ICU, GPA greater than 3.0, and a minimum score on an entrance exam such as
the Graduate Record Exam. Graduating student nurse anesthetist are trained
with a minimum of seven years of education and experience, completed
approximately 2,500 clinical hours and provided approximately 850
anesthetics to patients. After passing the national certification exam, the
CRNA must maintain his or her certification by completing new recertification
requirement consisting continuing education hours and passing a Continued
Professional Certification (CPC) exam every 8 years.
The scope of nurse anesthesia practice is governed by the Board of
Nursing and laws of the state in which the CRNA practices. The level of
supervision and scope of practice varies from state to state. CRNAs are
licensed advanced practice registered nurses (APRNs) and are trained to
“practice both autonomously and in collaboration with a variety of health
providers on the interprofessional team to deliver high-quality, holistic,
evidence-based anesthesia and pain care services.” As of 2016, 17 states
choose to “opt out” of the federal physician supervision requirement under the
Federal Medicare and Medicaid physician supervision requirement for
Certified Registered Nurse Anesthetists (CRNAs). This ruling states “that
regardless of whether a state "opts-out" of the federal supervision requirement,
individual facilities may still require CRNAs to be physician supervised.” The
rule goes on to state “that an opt-out would not permit a CRNA to practice
outside the scope of authority granted by state law. Nor would an opt-out
prohibit, limit, or restrict in any way the practice of medicine by a physician or
an anesthesiologist.” The topic of supervision of CRNA practice is a tenuous
subject where CRNAs and anesthesiologists continue to disagree.
Nurse anesthetists are trained in all aspects of anesthesia care and practice
in varied setting such as trauma centers, regional hospitals, small rural
hospital, surgery centers and physician offices. The AANA Scope of Practice
statement asserts “Nurse anesthesia practice may include, but is not limited to,
these elements: performing a comprehensive history and physical; conducting
a preanesthesia evaluation; obtaining informed consent for anesthesia;
developing and initiating a patient-specific plan of care; selecting, ordering,
prescribing and administering drugs and controlled substances; and selecting
and inserting invasive and noninvasive monitoring modalities. CRNAs provide
acute, chronic and interventional pain management services, as well as critical
care and resuscitation services; order and evaluate diagnostic tests; request
consultations; and perform point-of-care testing. CRNAs plan and initiate
anesthetic techniques, including general, regional, local, and sedation.
Anesthetic techniques may include the use of ultrasound, fluoroscopy and
other technologies for diagnosis and care delivery, and to improve patient
safety and comfort. Nurse anesthetists respond to emergency situations using

airway management and other techniques; facilitate emergence and recovery
from anesthesia; and provide post-anesthesia care, including medication
management, conducting a post-anesthesia evaluation, and discharge from the
post-anesthesia care area or facility.”
Another midlevel practitioner in the anesthesia field is the Anesthesia
Assistant (AA). The first AA training program enrolled students at Emory
University in 1969 in Atlanta, Georgia. There are 11 AA programs in 8 states
plus a program in the District of Columbia. The website for the American
Academy of Anesthesiologist Assistants (AAAA) organization list admission
lists the following requirements for admission to a CAA program as, “the
applicant must have achieved a bachelor's degree with prescribed prerequisites
typical of premedical course work. Specific requirements include general and
organic chemistry, advanced college math, general and advanced biology, and
physics.” The AA programs are 24-28 months long and AAs graduate having
earned a masters degree in anesthesia. In the United States there are
approximately 1500 Certified AAs practicing in 16 states plus the District of
Columbia. The AA scope of practice, while similar to the CRNA scope of
practice, is limited by the requirement of medical direction by an
anesthesiologist. This requirement precludes AAs from independent practice.
In conclusion, Nurse Anesthetists in the United States have been
providing anesthesia for over 150 years. CRNAs work in the anesthesia care
model in many locations but also are “the sole anesthesia providers in most
rural hospitals in the United States.” Nurse anesthetists also have a long history
of service in the US Military providing anesthesia for the military as far back
as the American Civil War. While there have been “turf wars” between
anesthesiologists and nurse anesthetists for decades, and now also between
anesthesia assistants and nurse anesthetists, the certified registered nurse
anesthetist is an integral part in the provision of anesthesia care in the United
States and they will continue in this fashion in the decades to come.
REFERENCES
American Academy of Anesthesiologist Assistants. “Educational Program
Requirements.” Accessed January 2017. https://aaaa.memberclicks.net/
assets/docs/factsheets/aa%20training%20and%20education%20fact%20sh
eet%202016_header.pdf.
American Association of Nurse Anesthetists. 2017. “Historical Resources.”

Accessed January 2017. http://www.aana.com/resources2/archives-
library/Pages/Historical-Resources.aspx.
American Association of Nurse Anesthetists. 2017. “History of Anesthesia
with Emphasis on the Nurse Specialist.” Accessed January 2017.
http://www.aana.com/resources2/archives-library/Pages/History-of-
Anesthesia-With-Emphasis-on-the-Nurse-Specialist.aspx.
Lawrence CS. 1896. Sketch of Life and Labors of Miss Catherine S. Lawrence.
Accessed January 2017. Albany, NY: James B. Lyon, Printer.
https://archive.org/details/autobiographyske00lawr.
Chapter 10
MALIGNANT HYPERTHERMIA,
THE “DISEASE OF ANESTHESIA”
Gregory Rose1, MD, J. Thomas McLarney2, MD,

Zaki Hassan3, MB and Raeford Brown4, MD
1
Department of Anesthesiology, University of Kentucky College of
Medicine, Lexington, Kentucky, US
2
Anesthesiology Preoperative and Preprocedural Assessment Clinic,
Department of Anesthesiology, University of Kentucky College of
Medicine, Lexington, Kentucky, US
3
Anesthesiology and Surgery, Director of Simulation,
University of Kentucky Healthcare Enterprise;
Liver Transplant Anesthesia, Department of Anesthesiology,
University of Kentucky College of Medicine, Lexington, Kentucky, US
4
Anesthesiology and Pediatrics, Department of Anesthesiology,
A forty year old male comes to you for preoperative evaluation for
repair of an inguinal hernia. His history, review of systems, and physical
exam are otherwise unremarkable. However, he tells you his brother died
during a herniorrhaphy 10 years ago. The patient does not know the
details, but he was told his brother developed a very high fever after
induction of anesthesia. The patient is afraid he is “allergic to anesthesia”
like his brother was.
How will you approach the perioperative care of this patient?
118 Gregory Rose, J. Thomas McLarney, Zaki Hassan et al.
INTRODUCTION
Malignant hyperthermia (MH) is a pharmacogenetic disease process
causing an acute hypermetabolic state upon exposure to certain anesthetic
agents. These “triggering agents” include succinylcholine, and the potent
inhalational anesthetics, e.g., halothane, isoflurane, sevoflurane, and
desflurane. All other medications used in anesthetic practice, including nitrous
oxide, sedative-hypnotics, opiates, local anesthetics, and nondepolarizing
muscle relaxants are safe to use in those susceptible to MH.
When first described, hyperpyrexia was usually the first symptom of MH
noticed during an anesthetic [1]. However with current anesthesia monitoring,
elevated end-tidal carbon dioxide, dysrhythmias, and metabolic acidosis are
often seen before an increase in body temperature is appreciated.
PATHOPHYSIOLOGY AND SYMPTOMS

Malignant hyperthermia is caused by a defect in the membranes of skeletal
muscle. Specifically there is a defect in the ryanodine receptor (RYR1) [2].
This receptor is responsible for intracellular calcium release from the
sarcoplasmic reticulum. Massive release of calcium during contraction occurs
when the RYR1 receptor is exposed to a triggering agent [3]. A
hypermetabolic state is caused due to uncontrolled muscle contractions when
the large amount of intracellular calcium is released.
Symptoms under anesthesia include muscle contractions, rigidity,
hypercarbia, severe metabolic acidosis, tachycardia, arrhythmias,
hyperkalemia, along with elevated temperature. Skeletal muscle breakdown
can cause rhabdomyolysis and elevations in creatine kinase [4]. If no
metabolic acidosis is seen by blood gas analysis the clinician should re-
evaluate the diagnosis of MH.
Masseter muscle spasm is a condition sometimes linked to MH [5]. When
it occurs it is with the administration of succinylcholine at induction of
anesthesia, it may be an early sign of MH. Large elevations in creatine kinase
levels, e.g., over 10,000, can be seen with masseter muscle spasm. No
definitive studies have conclusively linked masseter spasm to MH. Masseter
spasm that is associated with elevations in carbon dioxide, dysrhythmias,
myoglobinuria, total body rigidity, and fever should be treated as MH, and the
procedure cancelled. With masseter spasm alone, without any other symptoms
Malignant Hyperthermia, the “Disease of Anesthesia” 119
consistent with MH, many clinicians would change to a nontriggering

anesthetic technique and proceed with surgery, because the advent of propofol
has made this conversion much easier to do.
MH usually occurs shortly after anesthetic induction, but can happen
anytime during the perianesthetic period [6]. A study by Litman, et al. looked
at cases from the North American Malignant Hyperthermia Registry and found
that 1.9% of MH occurred post-operatively, sometimes up to 12 hours after
initial exposure to the triggering agent [7].
HISTORY
Michael Denborough described a number of anesthetic related deaths in an
Australian family in Lancet in 1960 [1, 8]. The anesthetics in this report
included ether and halothane. At that time, anesthesia monitoring was based
less on physiologic monitoring and more on clinical observation. A rapid rise
in temperature was a common feature in all of the reported cases, and was
named malignant hyperpyrexia, or hyperthermia. Further case reports from
that decade came from the United States, Canada, and South Africa as well as
Australia.
The animal model for MH is a condition described in Landrace pigs in
1966 [9]. This breed of pig often exhibited sudden death accompanied with
rigidity and muscle breakdown during the stress of transport. Porcine stress
syndrome, as it was to be called, also caused a similar picture in this strain of
pigs during research in which pigs had received succinylcholine [10].
Subsequent research with this porcine model found that the antispasmodic
drug dantrolene effectively treated MH [11]. By the mid 1970s, dantrolene
was in use for episodes of MH in humans [12]. In 1982 the Malignant
Hyperthermia Association of the United States (MHAUS) was founded to
support study and increase education of this disease. Similar organizations are
in Europe and Australia.
EPIDEMIOLOGY
The exact incidence of malignant hyperthermia is not known. The number
of reported cases has increased over the last twenty years. It is unclear whether
this is due to an increase in diagnosis and reporting or to an increase in
incidence. The incidence varies not only from country to country, but from
region to region, state to state, and within individual states. This is believed to
be due to variations in the gene pool. As an example, Michigan, Nebraska,
West Virginia and Wisconsin are areas with a higher incidence in the United
States. MH occurs more frequently in males than females (58% to 42%,
respectively). Between 2001 and 2005, the occurrence of MH increased from
10.2 to 13.3 patients per million hospital discharges, while the mortality rate in
the same period decreased from 16.1% to 6.5% [13].
The only conditions that are known to have an association with MH are
central core disease, Evans Myopathy, and King-Denborough Syndrome, all
diseases of the skeletal muscle membrane [14].
MIMICS OF MALIGNANT HYPERTHERMIA

Several conditions can mimic malignant hyperthermia in the operating
room. Iatrogenic causes include heat gain from warming devices, and faulty
monitoring equipment giving false data relating to temperature and end-tidal
carbon dioxide levels [15]. In addition, a malfunctioning of anesthesia
machine one-way valves can increase inspired carbon dioxide, as can
exhausted carbon dioxide absorbent.
Other mimics can include thyroid storm, undiagnosed pheochro-
mocytoma, and sepsis [16]. Acute patient intoxication with cocaine or ecstasy
can increase body temperature [17]. Transfusion reactions can also cause
hyperpyrexia.
Rarely, infant male patients experience hyperkalemic cardiac arrest on
anesthesia induction with succinylcholine. These patients will almost always
have an occult muscular dystrophy, such as Duchenne’s, which has not yet
presented itself [18]. Treatment of this condition should focus on reversal of
the severe hyperkalemia; dantrolene is not beneficial.
Acutely, the best diagnostic tool any time malignant hyperthermia is
suspected is arterial blood gas analysis. If there is no metabolic acidosis, then
MH is highly unlikely.
Neurolept malignant syndrome is a condition related to use of
antipsychotic agents, and can present with symptoms much like MH, including
rigidity, hyperpyrexia, and rhabdomyolysis [19]. There is no connection with
anesthetic agents. These patients are not at an increased risk with
administration of anesthetics.
AWAKE TRIGGERING
Several reports beginning in 1980 have discussed individuals having
symptoms consistent with MH who were not exposed to anesthetics [20].
Heatstroke was the presenting condition, accompanied by muscle pain,
increased creatine kinase (CK), rhabdomyolysis, and even cardiovascular
collapse [21]. These are believed to be cases of “awake triggering” in
genetically predisposed individuals under stressful conditions. Patients, when
tested, were found to have positive caffeine-halothane contracture test. Heat
sensitivity, night sweats, cramping, mottled skin, low-grade fever, and
excessive sweating are also seen in those susceptible. Individuals with such
symptoms, especially with elevated CK and rhabdomyolysis should have
further workup to rule out malignant hyperthermia. The treatment of an awake
episode of MH would include dantrolene and management of the other
symptoms seen acutely [22].
TREATMENT
Dantrolene is the specific and effective treatment for MH; it inhibits the
release of calcium from the sarcoplasmic reticulum of skeletal muscle by
limiting the activation of the ryanodine receptor [2]. Dantrolene should be
administered intravenously immediately after a diagnosis of MH is made.
During an acute episode of MH, triggering anesthetics should be
discontinued immediately as dantrolene is started. Anesthesia should be
maintained using non-triggering agents, and the surgery should be concluded
as rapidly as possible. The initial treatment with dantrolene is 2.5 milligrams
per kilogram intravenously and can be repeated every 5 to 10 minutes until the
patient stabilizes. Because of its poor water solubility the preparation of
dantrolene is tedious. One to two minutes is needed for it to dissolve in
solution. Extra staff should be utilized to mix the many vials that are needed to
treat an MH episode. For instance, a 70 kg person would require nine vials to
be mixed and administered for the initial dose.
The patient should be cooled with cold intravenous fluids, cold fluid
gastric lavage, chilled irrigations fluids, and packing in ice. It should be
remembered, however that dantrolene, not cooling, is the primary treatment.
Additional treatment is in response to the sequellae of MH, including
treatment of acidosis, arrhythmias, electrolyte disturbances, coagulopathy,

excess myoglobin, and acute renal failure.
Postoperatively these patients need to be monitored in an intensive care
setting. Recommendations are that patients be treated with dantrolene every 4
hours for 24 hours after the episode abates. Critical care monitoring is needed
because recrudescence of MH is seen in up to one fourth of patients.
Dantrolene itself can cause sedation and muscle weakness requiring
mechanical ventilation for several hours.
TESTING
Malignant hyperthermia susceptibility is tested in-vitro with the caffeine-
halothane contracture test (CHCT). This test is 97% sensitive and is 78%
specific, and is considered the gold standard for MH testing [23]. The CHCT
requires a fresh muscle biopsy, taken from the vastus lateralis; therefore it is
an invasive procedure, requiring an anesthetic, and is only done at special
centers in the United States. There are currently only four centers in North
America that perform this test. Children under 40 kilograms or ten years of age
are rarely tested, because of the size of the specimen required to perform the
test.
Molecular genetics testing should not be used as a screening test, because
a specific point mutation in the RYR1 receptor protein will be found in only
35% of patients, thereby missing 65% of positive subjects. Molecular testing is
appropriate for relatives of a subject who has had a positive genetic test in lieu
of undergoing the CHCT.
PERIOPERATIVE TREATMENT OF
A KNOWN MH SUSCEPTIBLE PATIENT
A patient with a known or highly suspicious risk of malignant

hyperthermia can safely be anesthetized for any surgical procedure. Close
cooperation and communication between the anesthesiologist and surgeon is
highly desirable, in order to avoid delays on the day of surgery. An
anesthesiologist who learns in the holding room of an elective case in which
the patient is an MH risk will have had no time to prepare for a non-triggering
anesthetic [24, 25]. Many facilities use specific anesthesia machines reserved
for these cases that are not equipped with inhalational triggering agent
vaporizers. These machines have been flushed for long periods to remove any
traces of volatile agent. Another option is the use of activated charcoal filters
on the breathing circuit of a regular anesthesia machine that has not been
flushed for a long period of time (Vapor-Clean, Dynasthetics, Salt Lake City,
Utah). Studies show that the filters remove enough agent from a “dirty”
machine to be safe for a susceptible patient [26].
Attempts to use dantrolene prophylactically to prevent MH in a
susceptible individual have been tried but are not advised currently. It has been
shown to be of no value to prophylactically treat a susceptible patient with
dantrolene.
For procedures requiring a general anesthetic, a non-triggering technique
incorporating infusions of propofol, remifentanil, sufentanil, or boluses of
narcotics with or without nitrous oxide is safe. Muscle relaxation to facilitate
surgery can safely be obtained by using any of the nondepolarizing relaxants
instead of succinylcholine.
Regional anesthetics, including neuraxial anesthesia and peripheral blocks
are excellent choices in appropriate procedures. Monitored anesthesia care
(MAC), with local anesthesia and intravenous sedation will also be safe for the
patient.
In the outpatient or office-based setting, patients who are MH susceptible
can undergo anesthesia using nontriggering agents. Freestanding facilities that
plan on using triggering agents should, however, have enough dantrolene
immediately available onsite to treat an episode, keeping in mind that multiple
doses of dantrolene are usually required [27]. There should also be ice readily
available in addition to having enough staff to mix dantrolene.
COUNSELING
The affected individual and family members should be made to
understand the life threatening implications of malignant hyperthermia. It
should also be made clear that it is a familial condition and that it may present
on subsequent anesthetics after a completely normal prior exposure to
triggering agents. Sometimes the patient may mistakenly think MH is an
“allergy to anesthesia”, or an “allergy to succinylcholine”. It should be made
clear that with a non-triggering technique they can undergo a safe anesthetic.
Anesthesiologists and nurse anesthetists are well trained to manage these
patients without the use of triggering anesthetic agents.
First-degree relatives should be counseled about undergoing the CHCT.

Molecular testing is appropriate for relatives of a subject who has had a
positive genetic test [28, 29]. If the genetic testing of relatives is positive, the
relatives should be presumed to have MH, and should have a non-triggering
anesthetic in the future; a muscle biopsy and CHCT are not needed. However,
if the genetic test is negative, the CHCT should be considered or the patient
presumed to be MH susceptible.
If a non-triggering anesthetic can be administered easily, why then is
testing of relatives needed? Non-triggering anesthetic techniques e.g., TIVA
(total intravenous anesthesia) are more costly in terms of drug expense and
time involved. Moreover, because MH is so rare, non-triggering anesthetic
techniques are not routinely used. The problem arises when a family history is
unable to be obtained on a MH susceptible patient or relative for whatever
reason such as in the case of trauma or an emergency procedure, possibly
exposing the patient to an MH trigger. Of course, one could argue that an
untested relative of an MH patient should wear a medicalert bracelet and avoid
testing. The choice for testing however should be given to the patient. Affected
individuals and first-degree relatives (unless shown by testing not to carry the
genetic defect) should wear medicalert bracelets.
The Malignant Hyperthermia Association of the United States (MHAUS)
and its website, www.mhaus.org, is a tremendous resource for both families
and clinicians. The MH hotline (1-800-644-9737) is staffed around the clock
by expert anesthesiologists to offer support to medical professionals in
managing an MH crisis as it is happening or to answer perioperative anesthesia
questions. Their focus is on clinicians in the U.S. and Canada, but the
organization does have a telephone number for international callers-001 315-
464-7079. The British Malignant Hyperthermia Association’s hotline
telephone number is 07947 609 601.
CONCLUSION
Malignant Hyperthermia is not an allergic reaction to anesthetics. It is a
familial genetic disorder, which on exposure to certain anesthetic agents
causes uncontrolled release of calcium from the sarcoplasmic reticulum. This
produces a state of hypermetabolism which is an acute, life-threatening
emergency. Rapid diagnosis and treatment with the only known antidote,
dantrolene, reduces the mortality from 70% to 5-15%. If MH occurs
intraoperatively it is most important to initiate therapy as soon as the diagnosis
is suspected and to conclude the procedure as rapidly as possible. The

caffeine-halothane contracture test is still the only reliable diagnostic test. At
this time, genetic testing is not sensitive enough to be used as a screening test.
Patients with known or suspected MH should be anesthetized using a non-
triggering technique. Finally, patients and medical practitioners can learn more
about malignant hyperthermia from mhaus.org.
REFERENCES
[1] Denborough MA, and Lovell RRH. Anaesthetic deaths in a family.
Lancet 1960; ii: 45.
[2] Parness J, Wehrens XHT, and Marks AR (Eds): Ryanodine Receptors
Structure, function and dysfunction in clinical disease. Series:
Developments in Cardiovascular Medicine, Vol. 254.
[3] Zucchi R, and Ronca-Testoni S: The sarcoplasmic reticulum Ca2+
channel/ryanodine receptor: modulation by endogenous effectors, drugs
and disease states. Pharmacol Rev. 1997; 49(1):1-51.
[4] Hopkins PM. Malignant hyperthermia: advances in clinical management
and diagnosis. Br J Anaesth 2000; 85:118–28.
[5] Rawicz M, Brandom BW, and Wolf A: The Place of Suxamethonium in
Pediatric Anesthesia. Pediatric Anesthesia 2009; 19: 561–570.
[6] Firstenberg M, Abel E, Blais D, and Andritsos, M: Delayed Malignant
Hyperthermia after Routine Coronary Bypass. Ann Thorac Surg
2010;89:947– 8.
[7] Litman R, Flood C, Kaplan R, Kim Y, and Tobin J: Postoperative
Malignant Hyperthermia. An Analysis of Cases from the North
American Malignant Hyperthermia Registry. Anesthesiology 2008;
109:825–9.
[8] Denborough MA, Forster JF, Lovell RRH, Maplestone PA, and Villiers
JD: Anaesthetic deaths in a family. Br J Anaesth 1962; 34:395–6.
[9] Hall L, Woolf N, Bradley J, and Jolly D: Unusual reaction to
suxamethonium chloride. BMJ 1966; 2:1305.
[10] Stalder K, and Conatser G: Porcine Stress Syndrome and Its Effects on
Maternal, Feedlot and Carcass Quantitative and Qualitative Traits.
Agricultural Extension Service, University of Tennessee.
[11] Harrison G: Control of the Malignant Hyperpyrexic Syndrome in MHS
Swine using Dantrolene Sodium. Br. J. Anaesthesia 1975; 47: 62-65.
[12] Kolb M, Horne M, and Martz R: Dantrolene in human malignant

hyperthermia. Anesthesiology 1982; 56(4):254-62.
[13] Rosero E, Adesanya A, Timaran C, and Joshi G: Trends and Outcomes
of Malignant Hyperthermia in the United States, 2000 to 2005.
[14] Litman RS, and Rosenberg H: Malignant Hyperthermia: Update on
Susceptibility Testing. JAMA 2005;293(23):2918-2924.
[15] Tautz TJ, Urwyler A, and Antognini JF: Case Scenario: Increased End-
tidal Carbon Dioxide. Anesthesiology 2010; 112: (2) 440–446.
[16] Parness J, Herlich A, Torp KD, Larach MG, and Miller J: Non-
malignant Hyperthermia and Malignant Hyperthermia Confused. J Clin
Anesth. 2008 June; 20(4): 313–316.
[17] Hall AP, and Henry JA: Acute Toxic Effects of ‘Ecstasy’ (MDMA) and
Related Compounds: Overview of Pathophysiology and Clinical
Management. British Journal of Anaesthesia 2006; 96 (6): 678–85.
[18] Hayes J, Veyckemans F, and Bissonnette B: Duchenne Muscular
Dystrophy: an Old Anesthesia Problem Revisited. Pediatric Anesthesia
2008 18: 100–106.
[19] Strawn JR, Keck PE, and Caroff SN: Neuroleptic Malignant Syndrome.
Am J Psychiatry 2007. 164 (6): 870-876.
[20] Tobin JR, Jason DR, Nelson TE, and Sambuughin N: Malignant
hyperthermia and apparent heat stroke (Correspondence). JAMA 2001;
286:168.
[21] Hopkins PM: Is there a Link between Malignant Hyperthermia and
Exertional Heat Illness? Br J Sports Med 2007; 41:283–284.
[22] Denborough M: Malignant hyperthermia. Lancet 1998; 352: 1131–36.
[23] Allen GC, Larach MG, Kunselman AR: The Sensitivity and Specificity
of the Caffeine-Halothane Contracture Test: A Report from the North
American Malignant Hyperthermia Registry. Anesthesiology 1998; 88
(3): 579-588.
[24] Gunter JB, Ball J, and Than-Win S: Preparation of the Dräger Fabius
Anesthesia Machine for the Malignant–Hyperthermia Susceptible
Patient. Anesth Analg 2008; 107: 1936–45.
[25] McGraw TT, Keon TP. Malignant hyperthermia and the clean machine.
Can J Anaesth 1989; 36:530–2.
[26] Birgenheier N, Stoker R, Westenskow D, Orr J. Activated Charcoal
Effectively Removes Inhaled Anesthetics from Modern Anesthesia
Machines. Anesthesia and Analgesia 2011: 112 (6): 1363–1370.
[27] Rosenberg H: Malignant Hyperthermia in the Ambulatory Setting.

Seminars in Anesthesia, Perioperative Medicine, and Pain 2001: 20 (4);
270-274.
[28] Dirksen SJH, Brandom BW, Muldoon SM, and Rosenberg, H: Genetic
Testing to Evaluate Susceptibility to Malignant Hyperthermia. ASA
Newsletter 2009; 73 (5): 36-38.
[29] Levano S. Vukcevic M, Singer M, et al.: Increasing the Number of
Diagnostic Mutations in Malignant Hyperthermia. Human Mutation
2009; 30 (4): 590-598.
ABOUT THE EDITORS
Gregory L. Rose, M.D.

Professor
Gregory L. Rose, M.D., is a professor of anesthesiology at the University

Of Kentucky College Of Medicine in Lexington. He received his medical
degree and completed his anesthesiology residency at the University of
Kentucky, and has been on the faculty there for 25 years. His professional
interests include resident education, acute pain management, airway
management techniques, and mood disorders as a form of impairment in
anesthesiology.
J. Thomas McLarney, M.D.

Professor
Medical Director, Anesthesiology Preoperative
and Preprocedural Assessment Clinic
J. Thomas McLarney, M.D. is a professor of anesthesiology at the

University Of Kentucky College Of Medicine in Lexington. He received both
his undergraduate degree in Industrial Psychology and his medical degree
130 About the Editors
from the University of Kentucky. He completed his anesthesiology residency

at the University of Kentucky. He has been faculty within the Department of
Anesthesiology for over sixteen years and is Medical Director of the
Anesthesiology Preoperative Assessment Clinic. In addition he is Chair of the
department’s education committee and sits on their clinical competency
committee. He is also course coordinator for a month fourth year medical
student class entitled Transitions to Residency. His professional interests
include preoperative assessment and optimization, perioperative pain
management, and resident and medical student education.
LIST OF CONTRIBUTORS
Lori C. Kral Barton, MD

Assistant Professor
Brooke A. Bauer, MD
Resident Physician
Raeford E Brown, Jr., MD, FAAP

Professor of Anesthesiology and Pediatrics
Charles Jonathan Fletcher, APRN, CRNA, BSN, MSN

Staff Nurse Anesthetist
132 List of Contributors
Zaki-Udin Hassan, MBBS, MBA

Professor of Anesthesiology and Surgery
Director of Simulation, University of Kentucky Healthcare Enterprise
Director of Liver Transplant Anesthesia
Jeffery Oldham, MD
Assistant Professor
Benjamin J. Sloop, MD
Fellow, Division of Chronic Pain Management
Habib Srour, MD
Assistant Professor
INDEX
# C
2-chloroprocaine, 65 caffeine-halothane contracture test (CHCT),

121, 122, 124, 125
cancer pain, 92
A cardiac assessment, 10
cardiac output, 26, 50, 66, 74, 80
ablations, 91
center for disease control, 90
acetaminophen, 90
cervicogenic headaches, 91
ACLS, 68, 69, 80, 81
cesarean delivery, 62, 70, 72, 74, 76, 79, 83,
acute respiratory distress syndrome, 63
85, 87
advanced maternal age, 71, 72, 78
chiropractic care, 92
airway assessment, 7, 9
chronic back pain, 92
aldosterone, 51
chronic hypertension, 70, 72
american society of regional anesthesia and
chronic neuropathic pain, 92
pain management, 56
clear liquid, 101, 103, 105
amniotic fluid embolism, 79, 80, 87
coagulation factors, 51
anticoagulants, 56, 91
coagulopathy, 56, 74, 79, 91, 122
anticonvulsants, 73, 90
cognitive behavioral therapy, 92
antidepressants, 90
combined spinal epidural, 64, 65
aortocaval compression, 51
continuous spinal, 56, 58, 63
aspiration, 26, 53, 58, 62, 63, 68, 70, 71, 73,
continuous spinal analgesia, 58, 63
77, 79, 85, 99, 100, 101, 102, 103, 104
contracture, 121, 122, 124, 125
awake triggering, 121
Crawford Long, 1
creatine kinase, 118, 121
B critical care, ix, 2, 39, 95, 96, 97, 113, 114,
122
baclofen, 92 Curtis L. Mendelson, 63
breast milk, 101, 102, 105
butorphanol, 61, 84
134 Index
HELLP Syndrome, 73
D hematoma, 56, 91
high, 8, 11, 17, 27, 29, 37, 39, 41, 43, 45,
dantrolene, 119, 120, 121, 122, 123, 124,
46, 55, 61, 64, 68, 69, 70, 78, 79, 80, 81,
125, 126
97, 103, 104, 114, 117
diagnostic blocks, 91
high spinal, 69
dorsal column stimulation, 91
Horace Wells, 1
drug testing, 90
I
E
implantable device, 91
eclampsia, 62, 72, 73
intrathecal, 50, 56, 58, 59, 63, 68, 70, 91, 92
epidural, 27, 54, 55, 56, 57, 58, 63, 64, 65,
intrathecal drug delivery, 91, 92
66, 68, 69, 70, 74, 75, 77, 81, 83, 84, 85,
isoflurane, 27, 28, 29, 81, 118
86, 91
epidural anesthesia, 57, 65, 86
epidural blood patch, 68, 86 J
epidural steroid injections, 91
epidural test dosing, 58 joint injections, 91
exercise, 82, 92, 112
L
F
local anesthetic, 45, 56, 64, 65, 66, 69, 92,
facet joint injection, 91 118
failed, 2, 62, 64, 68, 69, 70, 75, 77, 85, 86, local anesthetic systemic toxicity, 64, 68
92 local anesthetics, 45, 56, 65, 66, 69, 92, 118
failed back surgery syndrome, 92 Long, Crawford, 1
fentanyl, 29, 30, 31, 43, 61, 65, 75, 84, 85 low back pain, 91, 92
first stage of labor, 54, 84
fluid, 79, 80, 87
functional residual capacity, 50, 71 M
magnesium sulfate, 73, 74

G malignant hyperthermia, 44, 118, 119, 120,
121, 122, 123, 125, 126
geniculate nerve block, 91 malignant hyperthermia association of the
gestational diabetes mellitus, 72 United States (MHAUS), 119, 124
gestational hypertension, 72, 75 masseter muscle spasm, 118
glomerular filter rate, 53 maternal obesity, 70
medial branch nerve block, 91
medication management, 5, 17, 89, 115
H Mendelson, Curtis L., 63
meperidine, 60, 61, 84
halothane, 81, 118, 119, 126
minimal alveolar concentration, 49
HELLP, 51, 72, 73, 74
morphine, 30, 31, 60, 61, 65, 84
Index 135
Morton, William, 2 preeclampsia, 51, 53, 70, 72, 73, 74, 75, 86,
muscle relaxant(s), 73, 74, 90, 118 87
preoperative testing, 18, 19
primary care provider, 4, 37, 38, 40, 44, 46,
N 92
progesterone, 49, 50, 52, 53
nalbuphine, 61, 84
prostacyclin, 50, 82
narcotic, 24, 30, 31, 60, 90
pulmonary aspiration, 71, 86, 100, 104, 105
nerve, 89, 91
neuraxial anesthesia, 55, 56, 62, 63, 64, 70,
73, 74, 77, 79, 123 R
neurolept malignant syndrome, 120
neuromodulation, 91 receptor, 118, 121, 122, 125
neuropathic agents, 90 relaxin, 50, 52, 82
Nil per os, 99 remifentanil, 24, 30, 31, 61, 75, 123
nitrous oxide, 1, 27, 59, 64, 84, 107, 110, renin angiotensin aldosterone system, 51
118, 123 retained placenta, 75
NSAIDs, 90 rhabdomyolysis, 24, 118, 120, 121
rhizotomies, 89
ryanodine receptor (RYR1), 118, 121, 122,
O 125
opioid(s), 23, 25, 29, 30, 31, 34, 53, 58, 59,
60, 61, 64, 65, 66, 69, 85, 90, 92 S
oxytocin, 64, 74
sarcoplasmic reticulum, 118, 121, 124, 125
second stage of labor, 54
P sevoflurane, 27, 28, 46, 59, 84, 118
single nerve root injection, 91
pain management, 2, 59, 89, 96, 113, 114,
smoking cessation, 16, 21, 92
129, 130
spasticity, 92
patient controlled analgesia, 60, 61
spinal anesthetics, 65
perimortem cesarean section, 81
spinal cord stimulation, 91
perioperative medicine, 95, 96, 97
succinylcholine, 32, 33, 64, 118, 119, 120,
perioperative surgical home, 2, 97
123
peripheral nerve blocks, 89
physical therapy, 15, 89, 92
pill counts, 90 T
placenta accreta, 74, 75, 76, 78
placenta increta, 76 third occipital nerve, 91
placenta percreta, 76, 77 thrombocytopenia, 51, 56, 72, 82
placenta previa, 62, 72, 77, 78 thromboelastogram, 51, 74
placental abruption, 62, 72, 78, 79, 87 total spinal, 68, 69
post-dural puncture headache(s), 65, 66, 67, transforaminal epidural steroid injection, 91
83 transient neurological symptoms, 66
postpartum hemorrhage, 70, 74 triggering agents, 118, 121, 123
136 Index
U W
uterine blood flow, 51, 55, 57, 87 weight loss, 92

uterine rupture, 62, 74, 78 Wells, Horace, 1
William Morton, 2
World Health Organization (WHO), 90, 92
V
Vasa previa, 79, 87

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Library of Congress Cataloging-in-Publication Data

ISBN: 9 H%RRN

Published by Nova Science Publishers, Inc. † New York

Chapter 10 Malignant Hyperthermia, the “Disease of

Anesthesiology is one of the least understood medical specialties. The

In our role as academic anesthesiologists, we time and time again

THE SCOPE OF ANESTHESIA

What would the practice of modern medicine be like without

extractions on a series of patients but his demonstration at Massachusetts

capabilities and different time constraints. For instance, a preanesthetic

Table 1. ASA Physical Status Classification

Figure 1. ASA Difficult Airway Algorithm.

The purpose of the Guidelines is to facilitate the management of the

Figure 2. Mallampati Classification.

The Mallampati Classification [6] is a way to assess mouth opening

lead to management changes like what type of procedure is performed or when

Figure 3. Stepwise Approach to Perioperative Cardiac Assessment.

In a review on perioperative myocardial infarction published in 2009 in

Figure 4. Metabolic Equivalents.

Management of Patients with Implantable Defibrillators, Pacemakers and

Table 2. Preoperative recommendations

Communication is clearly key in the safe perioperative management of

also be concerned about the risk of bronchospasm or laryngospasm during the

Table 3. Essential elements of the information given to

Table 4. Essential elements of the preoperative CIED evaluation to be

From the ACP Guidelines, preoperative risk reduction strategies include

reasonable to delay surgery if possible to treat underlying pulmonary infection

communication with the patients PCP or endocrinologist is critical, especially

Testing in the preoperative period should be dictated by what is

[13] POISE Study Group. Effects of extended-release metoprolol succinate in

Noncardiothoracic Surgery: A guideline from the American College of

ANESTHETIC DRUGS FOR

Propofol is one of the most commonly administered induction agents in

properties [1]. Propofol is insoluble in water and therefore must be formulated

Etomidate is a carboxylated imidazole-containing compound that is

Ketamine is structurally similar to phencyclidine (the recreational drug

The cardiovascular effects of ketamine are very different from other

Midazolam is a short acting benzodiazepine frequently used for anxiolysis

properties in addition to anxiolysis. Mechanism of action involves binding to

anesthetics with neurotransmitter gated ion channels such as GABA, glycine

Inhalational induction of anesthesia occurs when the patient breathes a mixture

anesthesia at doses of 2-6 mcg/kg IV [6] to blunt the sympathetic response to

in airway management as there is a very small margin of error in regard to

contraction. The ACh is metabolized by acetylcholinesterase enzymes

of large doses of rocuronium (1.2 mg/kg) may approximate the speed of

muscarinic ACh peripheral receptors while having no effect at the nicotine

[9] Komatsu R, You J, Mascha EJ, Sessler DI, Kasuya Y, Turan A. A

Raeford E. Brown, Jr., MD, FAAP

in safe perioperative care. Also, I hope to reveal to the pediatric community

Pediatric Anesthesiologists think of themselves, on their best day, as the

1) The developmental level of the child – The operating room is a

a business card so that when questions come up in the preoperative

evaluation and management in the perioperative period. Infants that

PREOPERATIVE BEHAVIORAL STRESS IN CHILDREN

While the degree of change in observable physiologic parameters has been

It is a fact that children of anxious parents tend to be more anxious.

Social Adaptability or Coping Style

Children deal with the stresses of life in a variety of different ways.

Children with Previous Medical Experience

The use of anxiolytic compounds, such as benzodiazepines, for the

ISBN: 9 H%RRN